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    Name:
    Recombinant Rat FGF 10 Protein CF
    Description:
    The Recombinant Rat FGF 10 Protein from R D Systems is derived from E coli The Recombinant Rat FGF 10 Protein has been validated for the following applications Bioactivity
    Catalog Number:
    7804-fg-025/cf
    Price:
    259
    Applications:
    Bioactivity
    Purity:
    >95%, by SDS-PAGE under reducing conditions and visualized by silver stain
    Conjugate:
    Unconjugated
    Size:
    25 ug
    Category:
    Proteins and Enzymes
    Source:
    E. coli-derived Recombinant Rat FGF-10 Protein
    Buy from Supplier


    Structured Review

    R&D Systems fgf10
    Failed palate elevation associated with heightened tongue in mice overexpressing <t>Fgf10</t> in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened
    The Recombinant Rat FGF 10 Protein from R D Systems is derived from E coli The Recombinant Rat FGF 10 Protein has been validated for the following applications Bioactivity
    https://www.bioz.com/result/fgf10/product/R&D Systems
    Average 95 stars, based on 76 article reviews
    Price from $9.99 to $1999.99
    fgf10 - by Bioz Stars, 2020-09
    95/100 stars

    Images

    1) Product Images from "Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *"

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.432286

    Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened
    Figure Legend Snippet: Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened

    Techniques Used: Mouse Assay

    Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions
    Figure Legend Snippet: Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions

    Techniques Used: Mouse Assay, Over Expression, Labeling

    Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in
    Figure Legend Snippet: Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in

    Techniques Used: Inhibition, Expressing, Immunostaining, Mutagenesis

    FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation
    Figure Legend Snippet: FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation

    Techniques Used: Organ Culture, Labeling, Inhibition

    2) Product Images from "Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development"

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.079236

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal
    Figure Legend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Techniques Used:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,
    Figure Legend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Techniques Used: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5
    Figure Legend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Techniques Used: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,
    Figure Legend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Techniques Used: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding
    Figure Legend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Techniques Used: Staining

    3) Product Images from "Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development"

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.079236

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal
    Figure Legend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Techniques Used:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,
    Figure Legend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Techniques Used: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5
    Figure Legend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Techniques Used: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,
    Figure Legend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Techniques Used: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding
    Figure Legend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Techniques Used: Staining

    4) Product Images from "Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development"

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.079236

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal
    Figure Legend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Techniques Used:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,
    Figure Legend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Techniques Used: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5
    Figure Legend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Techniques Used: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,
    Figure Legend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Techniques Used: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding
    Figure Legend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Techniques Used: Staining

    5) Product Images from "Modeling human early otic sensory cell development with induced pluripotent stem cells"

    Article Title: Modeling human early otic sensory cell development with induced pluripotent stem cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0198954

    Schematic summary outlining the otic differentiation from hiPSCs in monolayer culture. (A) As a first step (step1), hiPSCs at day 0 were exposed to FGF3 and FGF10 growth factors until day 13 for early otic/placodal induction and, in a second step (step2) were then differentiated into otic sensory cells by exposure to either RA/EGF or DBZ until day 20. (B-D) Morphological characteristics of hiPSC-derived otic progenitor cells after FGF3/10, RA/EGF and DBZ treatments respectively. Scale bars, 200 μm. Abbreviations: DFNB, DMEM/F12 supplemented with N2 and B27; RA, retinoic acid; DBZ, difluoro-benzeneacetamide; EGF, epithelial growth factor; FGF, fibroblast growth factor.
    Figure Legend Snippet: Schematic summary outlining the otic differentiation from hiPSCs in monolayer culture. (A) As a first step (step1), hiPSCs at day 0 were exposed to FGF3 and FGF10 growth factors until day 13 for early otic/placodal induction and, in a second step (step2) were then differentiated into otic sensory cells by exposure to either RA/EGF or DBZ until day 20. (B-D) Morphological characteristics of hiPSC-derived otic progenitor cells after FGF3/10, RA/EGF and DBZ treatments respectively. Scale bars, 200 μm. Abbreviations: DFNB, DMEM/F12 supplemented with N2 and B27; RA, retinoic acid; DBZ, difluoro-benzeneacetamide; EGF, epithelial growth factor; FGF, fibroblast growth factor.

    Techniques Used: Derivative Assay

    6) Product Images from "Modeling human early otic sensory cell development with induced pluripotent stem cells"

    Article Title: Modeling human early otic sensory cell development with induced pluripotent stem cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0198954

    Schematic summary outlining the otic differentiation from hiPSCs in monolayer culture. (A) As a first step (step1), hiPSCs at day 0 were exposed to FGF3 and FGF10 growth factors until day 13 for early otic/placodal induction and, in a second step (step2) were then differentiated into otic sensory cells by exposure to either RA/EGF or DBZ until day 20. (B-D) Morphological characteristics of hiPSC-derived otic progenitor cells after FGF3/10, RA/EGF and DBZ treatments respectively. Scale bars, 200 μm. Abbreviations: DFNB, DMEM/F12 supplemented with N2 and B27; RA, retinoic acid; DBZ, difluoro-benzeneacetamide; EGF, epithelial growth factor; FGF, fibroblast growth factor.
    Figure Legend Snippet: Schematic summary outlining the otic differentiation from hiPSCs in monolayer culture. (A) As a first step (step1), hiPSCs at day 0 were exposed to FGF3 and FGF10 growth factors until day 13 for early otic/placodal induction and, in a second step (step2) were then differentiated into otic sensory cells by exposure to either RA/EGF or DBZ until day 20. (B-D) Morphological characteristics of hiPSC-derived otic progenitor cells after FGF3/10, RA/EGF and DBZ treatments respectively. Scale bars, 200 μm. Abbreviations: DFNB, DMEM/F12 supplemented with N2 and B27; RA, retinoic acid; DBZ, difluoro-benzeneacetamide; EGF, epithelial growth factor; FGF, fibroblast growth factor.

    Techniques Used: Derivative Assay

    7) Product Images from "Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon"

    Article Title: Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon

    Journal: American journal of medical genetics. Part A

    doi: 10.1002/ajmg.a.33670

    RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml
    Figure Legend Snippet: RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing

    Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal
    Figure Legend Snippet: Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal

    Techniques Used: Expressing, In Situ Hybridization

    A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,
    Figure Legend Snippet: A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,

    Techniques Used: In Situ Hybridization, Reverse Transcription Polymerase Chain Reaction

    8) Product Images from "Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon"

    Article Title: Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon

    Journal: American journal of medical genetics. Part A

    doi: 10.1002/ajmg.a.33670

    RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml
    Figure Legend Snippet: RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing

    Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal
    Figure Legend Snippet: Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal

    Techniques Used: Expressing, In Situ Hybridization

    A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,
    Figure Legend Snippet: A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,

    Techniques Used: In Situ Hybridization, Reverse Transcription Polymerase Chain Reaction

    9) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    10) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    11) Product Images from "Specific Heparan Sulfate Structures Modulate FGF10-mediated Submandibular Gland Epithelial Morphogenesis and Differentiation *"

    Article Title: Specific Heparan Sulfate Structures Modulate FGF10-mediated Submandibular Gland Epithelial Morphogenesis and Differentiation *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M709995200

    Model of FGF10-HS interaction during SMG morphogenesis. End bud expansion involves binding of specific HS fragments with 2 -O- and either N -or 6- O -sulfation, either alone or in combination with endogenous epithelial cell HSPGs, to FGFR2b. Increased FGFR2b signaling results in increased gene expression of FGFR1b and Fgf1 , leading to proliferation, and increased Aqp5 , a marker of end bud epithelial differentiation. There also may be specific HS structures that bind FGFR1b/FGF1. Decreased FGFR2b and increased Sprouty expression, negative regulators of FGFR signaling, balance the increased FGFR2b signaling. HS fragments with 6- O -sulfation alone increase duct elongation and expression of duct markers ( e.g. Cp2L1 ).
    Figure Legend Snippet: Model of FGF10-HS interaction during SMG morphogenesis. End bud expansion involves binding of specific HS fragments with 2 -O- and either N -or 6- O -sulfation, either alone or in combination with endogenous epithelial cell HSPGs, to FGFR2b. Increased FGFR2b signaling results in increased gene expression of FGFR1b and Fgf1 , leading to proliferation, and increased Aqp5 , a marker of end bud epithelial differentiation. There also may be specific HS structures that bind FGFR1b/FGF1. Decreased FGFR2b and increased Sprouty expression, negative regulators of FGFR signaling, balance the increased FGFR2b signaling. HS fragments with 6- O -sulfation alone increase duct elongation and expression of duct markers ( e.g. Cp2L1 ).

    Techniques Used: Binding Assay, Expressing, Marker

    Heparin oligosaccharides larger than dp10 increase BaF3/FGFR2b cell proliferation and SMG epithelial end bud expansion and morphogenesis. A , FGF10 (1 and 10 ng/ml) was added to BaF3/FGFR2b cells with 5 μg/ml sized heparin fragments. BaF3/FGFR2b cell proliferation begins to increase (2-fold) with 10 ng/ml FGF10 and dp10 heparin fragments and continues to increase as the saccharide size increases up to dp16, which is similar to heparin ( H ). B , SMG epithelia were cultured for 48 h with 200 ng/ml FGF10 (control) and 0.5 μg/ml sized heparin oligosaccharides. C , the number of buds, width of the end buds, and duct length were measured and combined to give a morphogenic index. At least five epithelia/condition were measured, and experiments were repeated three times (one-way analysis of variance compared with control: ** , p
    Figure Legend Snippet: Heparin oligosaccharides larger than dp10 increase BaF3/FGFR2b cell proliferation and SMG epithelial end bud expansion and morphogenesis. A , FGF10 (1 and 10 ng/ml) was added to BaF3/FGFR2b cells with 5 μg/ml sized heparin fragments. BaF3/FGFR2b cell proliferation begins to increase (2-fold) with 10 ng/ml FGF10 and dp10 heparin fragments and continues to increase as the saccharide size increases up to dp16, which is similar to heparin ( H ). B , SMG epithelia were cultured for 48 h with 200 ng/ml FGF10 (control) and 0.5 μg/ml sized heparin oligosaccharides. C , the number of buds, width of the end buds, and duct length were measured and combined to give a morphogenic index. At least five epithelia/condition were measured, and experiments were repeated three times (one-way analysis of variance compared with control: ** , p

    Techniques Used: Cell Culture

    Chemical desulfation of heparin decreases FGF10-mediated BaF3/FGFR2b cell proliferation and influences SMG epithelial morphogenesis. A , BaF3/FGFR2b cells were cultured with FGF10 (10 ng/ml) and 0.5 or 5 μg/ml de- N -sulfated ( De-NS ), completely desulfated ( C-DS ), N -desulfated and reacetylated ( DNSRAC ), de-2 -O- sulfated ( De-2OS ), or de-6 -O- sulfated ( De-6OS ) heparin. Results are expressed as a percentage of cell proliferation compared with heparin. B , SMG epithelia were cultured with FGF10 ( Control ) and 0.5 μg/ml of heparin, chemically modified heparins, and HS. C , the number of buds, width of the end buds, and duct length were measured and combined to give a morphogenic index. Removal of any sulfates from heparin increases the morphogenic index, similar to heparan sulfate. Removal of all O -sulfates ( De-OS ) results in a morphogenic index similar to control. At least five epithelia/condition were measured, and experiments were repeated three times (one-way analysis of variance compared with control: ** , p
    Figure Legend Snippet: Chemical desulfation of heparin decreases FGF10-mediated BaF3/FGFR2b cell proliferation and influences SMG epithelial morphogenesis. A , BaF3/FGFR2b cells were cultured with FGF10 (10 ng/ml) and 0.5 or 5 μg/ml de- N -sulfated ( De-NS ), completely desulfated ( C-DS ), N -desulfated and reacetylated ( DNSRAC ), de-2 -O- sulfated ( De-2OS ), or de-6 -O- sulfated ( De-6OS ) heparin. Results are expressed as a percentage of cell proliferation compared with heparin. B , SMG epithelia were cultured with FGF10 ( Control ) and 0.5 μg/ml of heparin, chemically modified heparins, and HS. C , the number of buds, width of the end buds, and duct length were measured and combined to give a morphogenic index. Removal of any sulfates from heparin increases the morphogenic index, similar to heparan sulfate. Removal of all O -sulfates ( De-OS ) results in a morphogenic index similar to control. At least five epithelia/condition were measured, and experiments were repeated three times (one-way analysis of variance compared with control: ** , p

    Techniques Used: Cell Culture, Modification

    Oligosaccharide libraries with defined sulfation show that the position of sulfates increases end bud morphogenesis and FGFR1b expression. A , oligosaccharide libraries (dp10, 0.5 mg/ml) with defined sulfate groups were added to SMG epithelial cultures with FGF10 (200 ng/ml). B , the number and width of the end buds and length of the ducts were measured and combined to give a morphogenic index. C , oligosaccharides that increase end bud width also have increased FGFR1b expression, and the SMGs with the greatest combined morphogenesis also have increased Fgf1 expression. Gene expression was normalized to 29S and expressed as a -fold increase compared with the expression in the Ido2AOH-GlcNAc6OH-treated group. At least five epithelia/condition were measured, and the experiment was repeated three times (one-way analysis of variance compared with no sulfate group: ** , p
    Figure Legend Snippet: Oligosaccharide libraries with defined sulfation show that the position of sulfates increases end bud morphogenesis and FGFR1b expression. A , oligosaccharide libraries (dp10, 0.5 mg/ml) with defined sulfate groups were added to SMG epithelial cultures with FGF10 (200 ng/ml). B , the number and width of the end buds and length of the ducts were measured and combined to give a morphogenic index. C , oligosaccharides that increase end bud width also have increased FGFR1b expression, and the SMGs with the greatest combined morphogenesis also have increased Fgf1 expression. Gene expression was normalized to 29S and expressed as a -fold increase compared with the expression in the Ido2AOH-GlcNAc6OH-treated group. At least five epithelia/condition were measured, and the experiment was repeated three times (one-way analysis of variance compared with no sulfate group: ** , p

    Techniques Used: Expressing

    FGF10 induces heparin-dependent proliferation of BaF3 cells expressing FGFR2b, and FGF10-dependent SMG epithelial morphogenesis and proliferation are modulated by heparan sulfate. A , BaF3/FGFR1b cells ( open circles ) or FGFR2b ( filled circles ) were cultured with FGF10 and 5 μg/ml heparin. FGF10 increases BaF3/FGFR2b cell proliferation in a dose-dependent manner but does not induce BaF3/FGFR1b cells to proliferate. B , BaF3/FGFR2b cells were cultured with 1 ng/ml FGF10 and increasing concentrations of heparin. C , E13 SMG epithelia were cultured with increasing doses of FGF10 and HS. Increasing concentrations of FGF10 induce duct elongation, whereas HS induces end bud expansion. D , heparan sulfate (0.5 μg/ml) increases FGF10-mediated (200 ng/ml) proliferation throughout the epithelium resulting in end bud expansion. Images are single confocal slices through the end bud with bromodeoxyuridine labeling ( red ), α3 integrin ( green ), and nuclei ( blue ).
    Figure Legend Snippet: FGF10 induces heparin-dependent proliferation of BaF3 cells expressing FGFR2b, and FGF10-dependent SMG epithelial morphogenesis and proliferation are modulated by heparan sulfate. A , BaF3/FGFR1b cells ( open circles ) or FGFR2b ( filled circles ) were cultured with FGF10 and 5 μg/ml heparin. FGF10 increases BaF3/FGFR2b cell proliferation in a dose-dependent manner but does not induce BaF3/FGFR1b cells to proliferate. B , BaF3/FGFR2b cells were cultured with 1 ng/ml FGF10 and increasing concentrations of heparin. C , E13 SMG epithelia were cultured with increasing doses of FGF10 and HS. Increasing concentrations of FGF10 induce duct elongation, whereas HS induces end bud expansion. D , heparan sulfate (0.5 μg/ml) increases FGF10-mediated (200 ng/ml) proliferation throughout the epithelium resulting in end bud expansion. Images are single confocal slices through the end bud with bromodeoxyuridine labeling ( red ), α3 integrin ( green ), and nuclei ( blue ).

    Techniques Used: Expressing, Cell Culture, Labeling

    12) Product Images from "Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *"

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.432286

    Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened
    Figure Legend Snippet: Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened

    Techniques Used: Mouse Assay

    Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions
    Figure Legend Snippet: Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions

    Techniques Used: Mouse Assay, Over Expression, Labeling

    Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in
    Figure Legend Snippet: Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in

    Techniques Used: Inhibition, Expressing, Immunostaining, Mutagenesis

    FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation
    Figure Legend Snippet: FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation

    Techniques Used: Organ Culture, Labeling, Inhibition

    13) Product Images from "Fgf10 and Sox9 are essential for the establishment of distal progenitor cells during mouse salivary gland development"

    Article Title: Fgf10 and Sox9 are essential for the establishment of distal progenitor cells during mouse salivary gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.146019

    Model of Fgf10 and Sox9 function during salivary gland budding and branching morphogenesis. Sox9 is required for branching initiation by promoting the formation of distal epithelial progenitors and their proliferation. Mesenchymal Fgf10 maintains epithelial
    Figure Legend Snippet: Model of Fgf10 and Sox9 function during salivary gland budding and branching morphogenesis. Sox9 is required for branching initiation by promoting the formation of distal epithelial progenitors and their proliferation. Mesenchymal Fgf10 maintains epithelial

    Techniques Used:

    Fgf10 maintains Sox9 expression during the initial stages of salivary gland development. (A-D) In situ hybridisation for Fgf10 (A,C) and Sox9 (B,D) on E11.0 mandibles (A,B) and frontal mandibular slices (C,D). Arrowheads indicate the site of expression
    Figure Legend Snippet: Fgf10 maintains Sox9 expression during the initial stages of salivary gland development. (A-D) In situ hybridisation for Fgf10 (A,C) and Sox9 (B,D) on E11.0 mandibles (A,B) and frontal mandibular slices (C,D). Arrowheads indicate the site of expression

    Techniques Used: Expressing, In Situ, Hybridization

    14) Product Images from "Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors"

    Article Title: Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20022135

    Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.
    Figure Legend Snippet: Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.

    Techniques Used: Polymerase Chain Reaction, Isolation, Purification, Expressing, BrdU Incorporation Assay, Cell Culture

    15) Product Images from "Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors"

    Article Title: Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20022135

    Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.
    Figure Legend Snippet: Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.

    Techniques Used: Polymerase Chain Reaction, Isolation, Purification, Expressing, BrdU Incorporation Assay, Cell Culture

    16) Product Images from "Guidance of Postural Motoneurons Requires MAPK/ERK Signaling Downstream of Fibroblast Growth Factor Receptor 1"

    Article Title: Guidance of Postural Motoneurons Requires MAPK/ERK Signaling Downstream of Fibroblast Growth Factor Receptor 1

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4932-09.2010

    FGF8 phosphorylates ERK in motoneurons derived from HBG3 and FGFR1 +/− but not FGFR1 −/− ES cells. A representative Western blot loaded with equal amounts of whole-cell lysate from motoneurons derived from HBG3, FGFR1 +/− , and FGFR1 −/− ES cells treated for 15 min with FGF8 (50 ng/ml), FGF10 (50 ng/ml), or media alone. p-ERK (1st row) and p-Akt (3rd row). Blots were reprobed with an antibody against total ERK (2nd row) or total Akt (4th row).
    Figure Legend Snippet: FGF8 phosphorylates ERK in motoneurons derived from HBG3 and FGFR1 +/− but not FGFR1 −/− ES cells. A representative Western blot loaded with equal amounts of whole-cell lysate from motoneurons derived from HBG3, FGFR1 +/− , and FGFR1 −/− ES cells treated for 15 min with FGF8 (50 ng/ml), FGF10 (50 ng/ml), or media alone. p-ERK (1st row) and p-Akt (3rd row). Blots were reprobed with an antibody against total ERK (2nd row) or total Akt (4th row).

    Techniques Used: Derivative Assay, Western Blot

    ES cell-derived MMCm motoneurons preferentially extend neurites toward FGF8 in 3-D collagen gels. A , B , ES cell-derived MMCm motoneurons preferentially extended eGFP + neurites toward FGF8-loaded beads after 24 h in culture, although they were equidistant to FGF10-loaded beads ( A ). ES cell-derived motoneurons lacking FGFR1 −/− , stained for β-III tubulin, did not show preference for either FGF8 or FGF10. Both images are a z -stack collapsed confocal image shown as an inverted black and white of the fluorescence. C , z -stack collapsed confocal images of the eGFP + ES cell-derived motoneurons, shown in A , immunolabeled for β-III tubulin. Merged image shows that the vast majority of neurites extending into the collagen are eGFP + and β-III tubulin + . Two eGFP − /β-III tubulin + neurites are indicated with arrowheads. D as supplemental material). Wild-type ES cell-derived motoneurons extended more neurites toward FGF8 compared with motoneurons lacking FGFR1 (ANOVA, p
    Figure Legend Snippet: ES cell-derived MMCm motoneurons preferentially extend neurites toward FGF8 in 3-D collagen gels. A , B , ES cell-derived MMCm motoneurons preferentially extended eGFP + neurites toward FGF8-loaded beads after 24 h in culture, although they were equidistant to FGF10-loaded beads ( A ). ES cell-derived motoneurons lacking FGFR1 −/− , stained for β-III tubulin, did not show preference for either FGF8 or FGF10. Both images are a z -stack collapsed confocal image shown as an inverted black and white of the fluorescence. C , z -stack collapsed confocal images of the eGFP + ES cell-derived motoneurons, shown in A , immunolabeled for β-III tubulin. Merged image shows that the vast majority of neurites extending into the collagen are eGFP + and β-III tubulin + . Two eGFP − /β-III tubulin + neurites are indicated with arrowheads. D as supplemental material). Wild-type ES cell-derived motoneurons extended more neurites toward FGF8 compared with motoneurons lacking FGFR1 (ANOVA, p

    Techniques Used: Derivative Assay, Staining, Fluorescence, Immunolabeling

    17) Product Images from "Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon"

    Article Title: Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon

    Journal: American journal of medical genetics. Part A

    doi: 10.1002/ajmg.a.33670

    RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml
    Figure Legend Snippet: RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing

    Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal
    Figure Legend Snippet: Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal

    Techniques Used: Expressing, In Situ Hybridization

    A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,
    Figure Legend Snippet: A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,

    Techniques Used: In Situ Hybridization, Reverse Transcription Polymerase Chain Reaction

    18) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    19) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    20) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    21) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    22) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    23) Product Images from "TGF-? mediated FGF10 signaling in cranial neural crest cells controls development of myogenic progenitor cells through tissue-tissue interactions during tongue morphogenesis"

    Article Title: TGF-? mediated FGF10 signaling in cranial neural crest cells controls development of myogenic progenitor cells through tissue-tissue interactions during tongue morphogenesis

    Journal: Developmental Biology

    doi: 10.1016/j.ydbio.2010.02.030

    Exogenous FGF10 rescues the reduction of muscle cells in Wnt1-Cre;Tgfbr2 flox/flox mice
    Figure Legend Snippet: Exogenous FGF10 rescues the reduction of muscle cells in Wnt1-Cre;Tgfbr2 flox/flox mice

    Techniques Used: Mouse Assay

    Fgf10 expression analysis in the developing tongue
    Figure Legend Snippet: Fgf10 expression analysis in the developing tongue

    Techniques Used: Expressing

    24) Product Images from "Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon"

    Article Title: Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon

    Journal: American journal of medical genetics. Part A

    doi: 10.1002/ajmg.a.33670

    RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml
    Figure Legend Snippet: RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing

    Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal
    Figure Legend Snippet: Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal

    Techniques Used: Expressing, In Situ Hybridization

    A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,
    Figure Legend Snippet: A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,

    Techniques Used: In Situ Hybridization, Reverse Transcription Polymerase Chain Reaction

    25) Product Images from "Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development"

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.079236

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal
    Figure Legend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Techniques Used:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,
    Figure Legend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Techniques Used: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5
    Figure Legend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Techniques Used: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,
    Figure Legend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Techniques Used: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding
    Figure Legend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Techniques Used: Staining

    26) Product Images from "Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development"

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.079236

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal
    Figure Legend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Techniques Used:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,
    Figure Legend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Techniques Used: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5
    Figure Legend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Techniques Used: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,
    Figure Legend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Techniques Used: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding
    Figure Legend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Techniques Used: Staining

    27) Product Images from "Fgf10 and Sox9 are essential for the establishment of distal progenitor cells during mouse salivary gland development"

    Article Title: Fgf10 and Sox9 are essential for the establishment of distal progenitor cells during mouse salivary gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.146019

    Model of Fgf10 and Sox9 function during salivary gland budding and branching morphogenesis. Sox9 is required for branching initiation by promoting the formation of distal epithelial progenitors and their proliferation. Mesenchymal Fgf10 maintains epithelial
    Figure Legend Snippet: Model of Fgf10 and Sox9 function during salivary gland budding and branching morphogenesis. Sox9 is required for branching initiation by promoting the formation of distal epithelial progenitors and their proliferation. Mesenchymal Fgf10 maintains epithelial

    Techniques Used:

    Fgf10 maintains Sox9 expression during the initial stages of salivary gland development. (A-D) In situ hybridisation for Fgf10 (A,C) and Sox9 (B,D) on E11.0 mandibles (A,B) and frontal mandibular slices (C,D). Arrowheads indicate the site of expression
    Figure Legend Snippet: Fgf10 maintains Sox9 expression during the initial stages of salivary gland development. (A-D) In situ hybridisation for Fgf10 (A,C) and Sox9 (B,D) on E11.0 mandibles (A,B) and frontal mandibular slices (C,D). Arrowheads indicate the site of expression

    Techniques Used: Expressing, In Situ, Hybridization

    28) Product Images from "Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors"

    Article Title: Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20022135

    Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.
    Figure Legend Snippet: Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.

    Techniques Used: Polymerase Chain Reaction, Isolation, Purification, Expressing, BrdU Incorporation Assay, Cell Culture

    29) Product Images from "Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors"

    Article Title: Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20022135

    Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.
    Figure Legend Snippet: Mesenchymal production of FGF7 and FGF10 regulate proliferation of embryonic thymic epithelium. Semiquantitative PCR (a) for FGF7, FGF10, and FGFR2IIIb was performed on cDNAs isolated from thymic epithelium, thymic mesenchyme and CD4 − 8 − thymocytes purified from E14 thymus. Equal loading of cDNA was monitored by analyzing β-actin mRNA expression. (b) Proliferation of thymic epithelium was analyzed by BrdU incorporation and Keratin expression in reaggregate cultures formed from whole E14 lobes, and from purified E14 thymic epithelium reaggregate cultures, the latter being cultured in the presence or absence of 100 ng/ml FGF7 and FGF10, either singularly or in combination. Experiments were performed three times with similar results.

    Techniques Used: Polymerase Chain Reaction, Isolation, Purification, Expressing, BrdU Incorporation Assay, Cell Culture

    30) Product Images from "Guidance of Postural Motoneurons Requires MAPK/ERK Signaling Downstream of Fibroblast Growth Factor Receptor 1"

    Article Title: Guidance of Postural Motoneurons Requires MAPK/ERK Signaling Downstream of Fibroblast Growth Factor Receptor 1

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4932-09.2010

    FGF8 phosphorylates ERK in motoneurons derived from HBG3 and FGFR1 +/− but not FGFR1 −/− ES cells. A representative Western blot loaded with equal amounts of whole-cell lysate from motoneurons derived from HBG3, FGFR1 +/− , and FGFR1 −/− ES cells treated for 15 min with FGF8 (50 ng/ml), FGF10 (50 ng/ml), or media alone. p-ERK (1st row) and p-Akt (3rd row). Blots were reprobed with an antibody against total ERK (2nd row) or total Akt (4th row).
    Figure Legend Snippet: FGF8 phosphorylates ERK in motoneurons derived from HBG3 and FGFR1 +/− but not FGFR1 −/− ES cells. A representative Western blot loaded with equal amounts of whole-cell lysate from motoneurons derived from HBG3, FGFR1 +/− , and FGFR1 −/− ES cells treated for 15 min with FGF8 (50 ng/ml), FGF10 (50 ng/ml), or media alone. p-ERK (1st row) and p-Akt (3rd row). Blots were reprobed with an antibody against total ERK (2nd row) or total Akt (4th row).

    Techniques Used: Derivative Assay, Western Blot

    ES cell-derived MMCm motoneurons preferentially extend neurites toward FGF8 in 3-D collagen gels. A , B , ES cell-derived MMCm motoneurons preferentially extended eGFP + neurites toward FGF8-loaded beads after 24 h in culture, although they were equidistant to FGF10-loaded beads ( A ). ES cell-derived motoneurons lacking FGFR1 −/− , stained for β-III tubulin, did not show preference for either FGF8 or FGF10. Both images are a z -stack collapsed confocal image shown as an inverted black and white of the fluorescence. C , z -stack collapsed confocal images of the eGFP + ES cell-derived motoneurons, shown in A , immunolabeled for β-III tubulin. Merged image shows that the vast majority of neurites extending into the collagen are eGFP + and β-III tubulin + . Two eGFP − /β-III tubulin + neurites are indicated with arrowheads. D as supplemental material). Wild-type ES cell-derived motoneurons extended more neurites toward FGF8 compared with motoneurons lacking FGFR1 (ANOVA, p
    Figure Legend Snippet: ES cell-derived MMCm motoneurons preferentially extend neurites toward FGF8 in 3-D collagen gels. A , B , ES cell-derived MMCm motoneurons preferentially extended eGFP + neurites toward FGF8-loaded beads after 24 h in culture, although they were equidistant to FGF10-loaded beads ( A ). ES cell-derived motoneurons lacking FGFR1 −/− , stained for β-III tubulin, did not show preference for either FGF8 or FGF10. Both images are a z -stack collapsed confocal image shown as an inverted black and white of the fluorescence. C , z -stack collapsed confocal images of the eGFP + ES cell-derived motoneurons, shown in A , immunolabeled for β-III tubulin. Merged image shows that the vast majority of neurites extending into the collagen are eGFP + and β-III tubulin + . Two eGFP − /β-III tubulin + neurites are indicated with arrowheads. D as supplemental material). Wild-type ES cell-derived motoneurons extended more neurites toward FGF8 compared with motoneurons lacking FGFR1 (ANOVA, p

    Techniques Used: Derivative Assay, Staining, Fluorescence, Immunolabeling

    31) Product Images from "Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon"

    Article Title: Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon

    Journal: American journal of medical genetics. Part A

    doi: 10.1002/ajmg.a.33670

    RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml
    Figure Legend Snippet: RT-PCR analysis showing rescue of Dlx expression by FGF. A, C). Cultures of periotic mesenchyme and otic epithelium were treated with excess RA (10 −6 M; days 1–7), then supplemented on day 2 with a combination of FGF3 and FGF10 (30 ng/ml

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing

    Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal
    Figure Legend Snippet: Expression of FGF3 and FGF10 coincides spatially and temporally with formation of the inner ear. A. Whole mount in situ hybridization showing FGF3 expression in the otic vesicle (OV) and developing vestibulo-acoustic ganglia (gVIII) at E10.25. B. Horizontal

    Techniques Used: Expressing, In Situ Hybridization

    A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,
    Figure Legend Snippet: A, B) Whole mount in situ hybridization of RA-exposed (B) and control (A) embryos, showing a diminution in FGF10 in the otocyst (demarcated by arrows) of the RA-exposed embryo in comparison to the control embryo. C-J) RT-PCR analysis confirmed these findings,

    Techniques Used: In Situ Hybridization, Reverse Transcription Polymerase Chain Reaction

    32) Product Images from "FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development"

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.062794

    Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic
    Figure Legend Snippet: Fgf10 and Fgf3 /SOX3 expression in the forming infundibulum and collar zone. ( A-C ) Anterior fp subpopulations (A and P) used in targeted fate mapping (A) were explanted and cultured in vitro (B) for 30 hours (E2.5 equivalent). The anterior (prosencephalic

    Techniques Used: Expressing, Cell Culture, In Vitro

    Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).
    Figure Legend Snippet: Collar cell descendants contribute to Fgf10 + infundibulum. ( A ) Boxed region indicates dissection of Fgf3 + collar zone cells. ( B-D ) Immediately after isolation, collar explants are Fgf3 + Fgf10 − (B,C) but are Fgf10 + after 24 hours in culture (D).

    Techniques Used: Dissection, Isolation

    FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected
    Figure Legend Snippet: FGF signalling promotes proliferating collar progenitors. ( A-E ) St 9 prosencephalic neck cells explanted and cultured in vitro. In control explants (B), collar cells expressing SOX3 and Fgf3 are detected after 48 hours, and an Fgf10 + protrusion is detected

    Techniques Used: Cell Culture, In Vitro, Expressing

    33) Product Images from "Induced pluripotent stem cells from GMP-grade hematopoietic progenitor cells and mononuclear myeloid cells"

    Article Title: Induced pluripotent stem cells from GMP-grade hematopoietic progenitor cells and mononuclear myeloid cells

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/scrt87

    Differentiation of blood-derived iPSCs in vitro and in vivo . (a) Blood-derived iPSC clones were spontaneously differentiated through embryoid body formation, and analyzed via immunocytochemistry for lineage markers for three embryonic germ layers (endoderm FOXA2, mesoderm CD31, and ectoderm β-III-tubulin). (b) Transplantation of iPSCs into renal capsule of SCID-beige mice resulted in teratoma formation. Tissue histology of teratomas demonstrated the cells of three germ layers including glandular, muscular, and neural rosette-like tissues. (c) Schematic diagram describing the stepwise-guided differentiation protocol for iPSC differentiation into islet-like cells. ActA, Activin A; CYC, cyclopamine; DE, definitive endoderm; FGF10, fibroblast growth factor 10; GLP-1, glucagon-like peptide-1; HGF1, hepatocyte growth factor-1; IGF, insulin-like growth factor-1; ILV, indolactam V; ISL, islet-like cells; PE, pancreatic endoderm; PG, primitive gut; RA, all- trans retinoic acid; Wnt, Wnt3a. (d) Through the guided differentiation protocol, HPC- or PBMC-derived iPSC clones were induced to definitive endoderm (day 5), pancreatic endoderm (day 10), and insulin-producing islet-like cells (day 24). Immunostaining demonstrated the expression of stage-specific markers in iPSC progeny at day 5 (FOXA2 and SOX17), day 10 (NKX6.1 and PDX1), and day 24 (INS). Scale bars indicate 50 μm.
    Figure Legend Snippet: Differentiation of blood-derived iPSCs in vitro and in vivo . (a) Blood-derived iPSC clones were spontaneously differentiated through embryoid body formation, and analyzed via immunocytochemistry for lineage markers for three embryonic germ layers (endoderm FOXA2, mesoderm CD31, and ectoderm β-III-tubulin). (b) Transplantation of iPSCs into renal capsule of SCID-beige mice resulted in teratoma formation. Tissue histology of teratomas demonstrated the cells of three germ layers including glandular, muscular, and neural rosette-like tissues. (c) Schematic diagram describing the stepwise-guided differentiation protocol for iPSC differentiation into islet-like cells. ActA, Activin A; CYC, cyclopamine; DE, definitive endoderm; FGF10, fibroblast growth factor 10; GLP-1, glucagon-like peptide-1; HGF1, hepatocyte growth factor-1; IGF, insulin-like growth factor-1; ILV, indolactam V; ISL, islet-like cells; PE, pancreatic endoderm; PG, primitive gut; RA, all- trans retinoic acid; Wnt, Wnt3a. (d) Through the guided differentiation protocol, HPC- or PBMC-derived iPSC clones were induced to definitive endoderm (day 5), pancreatic endoderm (day 10), and insulin-producing islet-like cells (day 24). Immunostaining demonstrated the expression of stage-specific markers in iPSC progeny at day 5 (FOXA2 and SOX17), day 10 (NKX6.1 and PDX1), and day 24 (INS). Scale bars indicate 50 μm.

    Techniques Used: Derivative Assay, In Vitro, In Vivo, Clone Assay, Immunocytochemistry, Transplantation Assay, Mouse Assay, Immunostaining, Expressing

    34) Product Images from "Monoclonal Antibodies to Fibroblast Growth Factor Receptor 2 Effectively Inhibit Growth of Gastric Tumor Xenografts"

    Article Title: Monoclonal Antibodies to Fibroblast Growth Factor Receptor 2 Effectively Inhibit Growth of Gastric Tumor Xenografts

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    doi: 10.1158/1078-0432.CCR-10-0531

    ELISA measuring inhibition of binding of FGF2 ( A ), FGF7 ( B ) and FGF10 ( C ) to FGFR2IIIb by mAbs GAL-FR21, GAL-FR22, GAL-FR23 (FGF10 only) and negative control mAb mIgG.
    Figure Legend Snippet: ELISA measuring inhibition of binding of FGF2 ( A ), FGF7 ( B ) and FGF10 ( C ) to FGFR2IIIb by mAbs GAL-FR21, GAL-FR22, GAL-FR23 (FGF10 only) and negative control mAb mIgG.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Inhibition, Binding Assay, Negative Control

    35) Product Images from "Intestinal Subepithelial Myofibroblasts Support in vitro and in vivo Growth of Human Small Intestinal Epithelium"

    Article Title: Intestinal Subepithelial Myofibroblasts Support in vitro and in vivo Growth of Human Small Intestinal Epithelium

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0026898

    In vivo Human Small Intestinal Enteroids Can Be Maintained with Murine ISEMFs. Human small intestinal crypts on murine myofibroblasts were grown in culture for 11 days in the presence of Wnt3a and FGF10, and then placed on a PGA felt scaffold and implanted subcutaneously into an immunocompromised NOD-SCID-IL2Rγ null mice. After 28 days, the implant was harvested and evaluated with intestinal epithelial markers. (A) H E demonstrates at least three cell morphologies, and eosinophilic material in the cyst lumen. (B) E-cadherin and (C) CDX-2, are intestinal epithelial cell markers. Again note the variable staining intensity by the CDX-2 suggestive of crypt and villus domains (D) α Smooth Muscle Actin staining for myofibroblast adjacent to epithelial cells. (E) PAS staining for mucin and mucin producing goblet cells (F) Chromogranin A, marker for enteroendocrine cells. For all images, scale bar is 100 µm.
    Figure Legend Snippet: In vivo Human Small Intestinal Enteroids Can Be Maintained with Murine ISEMFs. Human small intestinal crypts on murine myofibroblasts were grown in culture for 11 days in the presence of Wnt3a and FGF10, and then placed on a PGA felt scaffold and implanted subcutaneously into an immunocompromised NOD-SCID-IL2Rγ null mice. After 28 days, the implant was harvested and evaluated with intestinal epithelial markers. (A) H E demonstrates at least three cell morphologies, and eosinophilic material in the cyst lumen. (B) E-cadherin and (C) CDX-2, are intestinal epithelial cell markers. Again note the variable staining intensity by the CDX-2 suggestive of crypt and villus domains (D) α Smooth Muscle Actin staining for myofibroblast adjacent to epithelial cells. (E) PAS staining for mucin and mucin producing goblet cells (F) Chromogranin A, marker for enteroendocrine cells. For all images, scale bar is 100 µm.

    Techniques Used: In Vivo, Mouse Assay, Staining, Marker

    Long-term In vitro Human Small Intestinal Enteroids Grown on Murine Myofibroblasts. Human small intestinal crypts cultured on murine myofibroblasts in the presence of Wnt3a and FGF10 were processed after 58 days in vitro . (A) Hematoxylin and Eosin stain. (B) CDX-2, stains intestinal epithelium. (C) E-cadherin, an epithelial cell marker. (D) α Smooth Muscle Actin, marker for myofibroblasts.
    Figure Legend Snippet: Long-term In vitro Human Small Intestinal Enteroids Grown on Murine Myofibroblasts. Human small intestinal crypts cultured on murine myofibroblasts in the presence of Wnt3a and FGF10 were processed after 58 days in vitro . (A) Hematoxylin and Eosin stain. (B) CDX-2, stains intestinal epithelium. (C) E-cadherin, an epithelial cell marker. (D) α Smooth Muscle Actin, marker for myofibroblasts.

    Techniques Used: In Vitro, Cell Culture, H&E Stain, Marker

    Supportive Effect of Wnt, FGF Growth Factors and Myofibroblasts on Human Epithelial Growth. (A) Human small intestinal crypts cultured without myofibroblasts (MFs) or growth factors (GFs) will live for approximately two days before dying off. (B) Human small intestinal crypts cultured in the presence of murine myofibroblast but without growth factors maintain their cystic shape indefinitely but without significant growth. (C) Human small intestinal crypts cultured with Wnt3a and FGF10 growth factors in the presence of mouse myofibroblasts began as simple cysts that fill and extruded their contents and became more complex in morphology over time. (D) Human epithelial clusters grown on adult human myofibroblasts in the presence of growth factors organize into simple cysts but cannot be maintained for longer than 3 days. (E) Infant human myofibroblasts are capable of supporting human intestinal epithelial growth into complex cystic structures through 9 days post-explantation. For A and B, scale bar is 200 µm. For C, D, and E, scale bar is 100 µm.
    Figure Legend Snippet: Supportive Effect of Wnt, FGF Growth Factors and Myofibroblasts on Human Epithelial Growth. (A) Human small intestinal crypts cultured without myofibroblasts (MFs) or growth factors (GFs) will live for approximately two days before dying off. (B) Human small intestinal crypts cultured in the presence of murine myofibroblast but without growth factors maintain their cystic shape indefinitely but without significant growth. (C) Human small intestinal crypts cultured with Wnt3a and FGF10 growth factors in the presence of mouse myofibroblasts began as simple cysts that fill and extruded their contents and became more complex in morphology over time. (D) Human epithelial clusters grown on adult human myofibroblasts in the presence of growth factors organize into simple cysts but cannot be maintained for longer than 3 days. (E) Infant human myofibroblasts are capable of supporting human intestinal epithelial growth into complex cystic structures through 9 days post-explantation. For A and B, scale bar is 200 µm. For C, D, and E, scale bar is 100 µm.

    Techniques Used: Cell Culture

    In vitro Human Small Intestinal Enteroids Grown on Murine Myofibroblasts Demonstrate Characteristic Intestinal Epithelial Markers. Human crypts cultured on murine myofibroblasts in the presence of Wnt3a and FGF10 were processed after 18 days in vitro . (A) Phase contrast microscopy of culture. (B) Hematoxylin and Eosin stain. Note cellular polarity with epithelial nuclei at the basal region and goblet cells at the apical region. (C) E-cadherin, an epithelial cell marker. (D) CDX-2, stains intestinal epithelium. Of note, while the E-cadherin staining is relatively even, the CDX-2 staining demonstrates uneven staining suggestive of alternating crypt-villus domains. (E) Smooth Muscle Actin, marker for myofibroblasts. (F) PAS, stains for goblet cells. Note the extruded mucinous material at the apical side of the epithelium culture. (G) Lysozyme, a Paneth cell marker. (H) Synaptophysin, marker for enteroendocrine cells. For all images, scale bars are 100 µm.
    Figure Legend Snippet: In vitro Human Small Intestinal Enteroids Grown on Murine Myofibroblasts Demonstrate Characteristic Intestinal Epithelial Markers. Human crypts cultured on murine myofibroblasts in the presence of Wnt3a and FGF10 were processed after 18 days in vitro . (A) Phase contrast microscopy of culture. (B) Hematoxylin and Eosin stain. Note cellular polarity with epithelial nuclei at the basal region and goblet cells at the apical region. (C) E-cadherin, an epithelial cell marker. (D) CDX-2, stains intestinal epithelium. Of note, while the E-cadherin staining is relatively even, the CDX-2 staining demonstrates uneven staining suggestive of alternating crypt-villus domains. (E) Smooth Muscle Actin, marker for myofibroblasts. (F) PAS, stains for goblet cells. Note the extruded mucinous material at the apical side of the epithelium culture. (G) Lysozyme, a Paneth cell marker. (H) Synaptophysin, marker for enteroendocrine cells. For all images, scale bars are 100 µm.

    Techniques Used: In Vitro, Cell Culture, Microscopy, H&E Stain, Marker, Staining

    36) Product Images from "Artificial three-dimensional niches deconstruct pancreas development in vitro"

    Article Title: Artificial three-dimensional niches deconstruct pancreas development in vitro

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.096628

    3D in vitro pancreas organogenesis relies on FGF and Notch signaling, similar to the embryonic pancreas. ( A-F ) Fluorescence imaging of nGFP driven by the Pdx1 promoter in the presence of FGFs (A-E), after removal of FGF10 (B), FGF1 (C), all exogenous
    Figure Legend Snippet: 3D in vitro pancreas organogenesis relies on FGF and Notch signaling, similar to the embryonic pancreas. ( A-F ) Fluorescence imaging of nGFP driven by the Pdx1 promoter in the presence of FGFs (A-E), after removal of FGF10 (B), FGF1 (C), all exogenous

    Techniques Used: In Vitro, Fluorescence, Imaging

    37) Product Images from "Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *"

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.432286

    Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened
    Figure Legend Snippet: Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened

    Techniques Used: Mouse Assay

    Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions
    Figure Legend Snippet: Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions

    Techniques Used: Mouse Assay, Over Expression, Labeling

    Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in
    Figure Legend Snippet: Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in

    Techniques Used: Inhibition, Expressing, Immunostaining, Mutagenesis

    FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation
    Figure Legend Snippet: FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation

    Techniques Used: Organ Culture, Labeling, Inhibition

    38) Product Images from "Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *"

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.432286

    Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened
    Figure Legend Snippet: Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened

    Techniques Used: Mouse Assay

    Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions
    Figure Legend Snippet: Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions

    Techniques Used: Mouse Assay, Over Expression, Labeling

    Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in
    Figure Legend Snippet: Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in

    Techniques Used: Inhibition, Expressing, Immunostaining, Mutagenesis

    FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation
    Figure Legend Snippet: FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation

    Techniques Used: Organ Culture, Labeling, Inhibition

    39) Product Images from "Wnt/?-catenin signaling promotes expansion of Isl-1-positive cardiac progenitor cells through regulation of FGF signaling"

    Article Title: Wnt/?-catenin signaling promotes expansion of Isl-1-positive cardiac progenitor cells through regulation of FGF signaling

    Journal: Journal of Clinical Investigation

    doi: 10.1172/JCI31731

    FGF10 is a direct target of Wnt/β-catenin signaling in the AHF. ( A ) The FGF10-AHF enhancer from the FGF10 gene contains 2 cross-species–conserved LEF/TCF DNA binding sites. ( B and C ) The FGF10-AHF enhancer is activated and repressed by an activated form of β-catenin (β-catenin 41A/45A ) and dominant-negative TCF3 (dnTCF2), respectively. ( D and E ) ChIP assays showed that β-catenin formed a complex on the FGF10-AHF enhancer in vivo ( D ), and LiCl treatment of 293 T cells increased the association of β-catenin with this enhancer element ( E ). ( F ) Model of Wnt/FGF signaling promoting expansion of Isl-1–positive AHF progenitors through activation of specific FGF ligands, leading to proliferation and proper development of the outflow tract and right ventricle of the heart.
    Figure Legend Snippet: FGF10 is a direct target of Wnt/β-catenin signaling in the AHF. ( A ) The FGF10-AHF enhancer from the FGF10 gene contains 2 cross-species–conserved LEF/TCF DNA binding sites. ( B and C ) The FGF10-AHF enhancer is activated and repressed by an activated form of β-catenin (β-catenin 41A/45A ) and dominant-negative TCF3 (dnTCF2), respectively. ( D and E ) ChIP assays showed that β-catenin formed a complex on the FGF10-AHF enhancer in vivo ( D ), and LiCl treatment of 293 T cells increased the association of β-catenin with this enhancer element ( E ). ( F ) Model of Wnt/FGF signaling promoting expansion of Isl-1–positive AHF progenitors through activation of specific FGF ligands, leading to proliferation and proper development of the outflow tract and right ventricle of the heart.

    Techniques Used: Binding Assay, Dominant Negative Mutation, Chromatin Immunoprecipitation, In Vivo, Activation Assay

    Regulation of AHF marker genes and progenitor number by Wnt signaling. ( A and B ) FGF10 and Hand2 expression was reduced specifically in the hearts of SM22cre/ Catnb flox/flox mutants (arrowheads). ( C ) Q-PCR was used to quantitate expression changes in the hearts of E9.5 SM22cre/ Catnb flox/flox mutants. Expression of FGF10 and Hand2 was significantly downregulated, while expression of cTnI and Nkx2.5 was not appreciably affected by loss of β-catenin. ( D – F ) To activate canonical Wnt signaling in vivo, developing embryos were treated with LiCl as described in Methods. LiCl treatment of embryos increased outflow tract (brackets) length. ( G and H ) This increased outflow tract length was associated with an increase in the number of Isl-1–positive AHF progenitors migrating into the outflow tract (brackets) and increased Isl-1 staining in the pharyngeal mesoderm harboring the Isl-1–positive AHF progenitor pool (arrows). ( I ) The number of Isl-1–positive cells in the outflow tract/right ventricle increased approximately 50% in Isl-1–positive AHF progenitors after LiCl treatment. ( J and K ) FGF10 and Hand2 expression was upregulated in the outflow tract and right ventricle after LiCl treatment (arrows). *** P
    Figure Legend Snippet: Regulation of AHF marker genes and progenitor number by Wnt signaling. ( A and B ) FGF10 and Hand2 expression was reduced specifically in the hearts of SM22cre/ Catnb flox/flox mutants (arrowheads). ( C ) Q-PCR was used to quantitate expression changes in the hearts of E9.5 SM22cre/ Catnb flox/flox mutants. Expression of FGF10 and Hand2 was significantly downregulated, while expression of cTnI and Nkx2.5 was not appreciably affected by loss of β-catenin. ( D – F ) To activate canonical Wnt signaling in vivo, developing embryos were treated with LiCl as described in Methods. LiCl treatment of embryos increased outflow tract (brackets) length. ( G and H ) This increased outflow tract length was associated with an increase in the number of Isl-1–positive AHF progenitors migrating into the outflow tract (brackets) and increased Isl-1 staining in the pharyngeal mesoderm harboring the Isl-1–positive AHF progenitor pool (arrows). ( I ) The number of Isl-1–positive cells in the outflow tract/right ventricle increased approximately 50% in Isl-1–positive AHF progenitors after LiCl treatment. ( J and K ) FGF10 and Hand2 expression was upregulated in the outflow tract and right ventricle after LiCl treatment (arrows). *** P

    Techniques Used: Marker, Expressing, Polymerase Chain Reaction, In Vivo, Staining

    FGF signaling is activated by Wnt signaling in the AHF. ( A and B ) ERK1/2 phosphorylation was used to assess the activity of FGF signaling in the AHF. SM22cre/ Catnb flox/flox mutants expressed less phosphorylated ERK1/2 in the AHF and outflow tract than did wild-type littermates at E9.5 (arrowheads). PO4, phosphorylation. ( C and D ) ERK1/2 phosphorylation increased in the outflow tract and right ventricular myocardium in SM22cre/ Catnb flox(ex3)/+ embryos at E10.5 (arrowheads). ( E ) FGF10 and FGF8 expression was assessed by Q-PCR in AHF explants treated with Wnt3a. Surprisingly, FGF10 expression was significantly upregulated, while expression of FGF8, which is also expressed in the AHF, was unchanged. Expression of both Isl-1 and Hand2 was upregulated as expected. ( F ) Expression of additional FGF ligands was determined by Q-PCR, and FGF3, FGF10, FGF16, and FGF20 were all significantly upregulated by Wnt3a treatment, whereas FGF4 was downregulated. ( G and H ) Activation of AHF gene expression ( G ) and Isl-1–positive AHF progenitor number ( H ) by Wnt3a was attenuated by the FGF receptor inhibitor SU5402, indicating that these pathways act cooperatively in regulating AHF development. ( I ) Conversely, Wnt3a and FGF10 cooperatively increased Isl-1 expression in AHF explants, further supporting interaction between Wnt and FGF signaling in AHF development. ** P
    Figure Legend Snippet: FGF signaling is activated by Wnt signaling in the AHF. ( A and B ) ERK1/2 phosphorylation was used to assess the activity of FGF signaling in the AHF. SM22cre/ Catnb flox/flox mutants expressed less phosphorylated ERK1/2 in the AHF and outflow tract than did wild-type littermates at E9.5 (arrowheads). PO4, phosphorylation. ( C and D ) ERK1/2 phosphorylation increased in the outflow tract and right ventricular myocardium in SM22cre/ Catnb flox(ex3)/+ embryos at E10.5 (arrowheads). ( E ) FGF10 and FGF8 expression was assessed by Q-PCR in AHF explants treated with Wnt3a. Surprisingly, FGF10 expression was significantly upregulated, while expression of FGF8, which is also expressed in the AHF, was unchanged. Expression of both Isl-1 and Hand2 was upregulated as expected. ( F ) Expression of additional FGF ligands was determined by Q-PCR, and FGF3, FGF10, FGF16, and FGF20 were all significantly upregulated by Wnt3a treatment, whereas FGF4 was downregulated. ( G and H ) Activation of AHF gene expression ( G ) and Isl-1–positive AHF progenitor number ( H ) by Wnt3a was attenuated by the FGF receptor inhibitor SU5402, indicating that these pathways act cooperatively in regulating AHF development. ( I ) Conversely, Wnt3a and FGF10 cooperatively increased Isl-1 expression in AHF explants, further supporting interaction between Wnt and FGF signaling in AHF development. ** P

    Techniques Used: Activity Assay, Expressing, Polymerase Chain Reaction, Activation Assay, Activated Clotting Time Assay

    40) Product Images from "Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development"

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.079236

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal
    Figure Legend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Techniques Used:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,
    Figure Legend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Techniques Used: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5
    Figure Legend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Techniques Used: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,
    Figure Legend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Techniques Used: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding
    Figure Legend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Techniques Used: Staining

    Related Articles

    other:

    Article Title: Dynamic relationship of the epithelium and mesenchyme during salivary gland initiation: the role of Fgf10
    Article Snippet: Fgf8 protein has been found localised to both the gland epithelium and mesenchyme at early stages of SMG development, and intriguingly the level of Fgf10 protein in the aborted glands was suggested to be reduced in conditional Fgf8 mutants ( ; ).

    Article Title: Retinoid Signaling in Inner Ear Development: a "Goldilocks" Phenomenon
    Article Snippet: Fgf3 and Fgf10 are required for mouse otic placode induction.

    Article Title: Dynamic relationship of the epithelium and mesenchyme during salivary gland initiation: the role of Fgf10
    Article Snippet: To test this, beads soaked in Fgf10 protein were placed close to the developing submandibular gland at the initial bud stage.

    Article Title: FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development
    Article Snippet: FGF10 maintains stem cell compartment in developing mouse incisors .

    Expressing:

    Article Title: Modeling human early otic sensory cell development with induced pluripotent stem cells
    Article Snippet: .. Indeed, ectopic expression of FGF3 or FGF10 during mouse embryogenesis induces the formation of ectopic otic vesicles expressing some otic markers i.e., PAX2 [ ]. ..

    Article Title: Modeling human early otic sensory cell development with induced pluripotent stem cells
    Article Snippet: .. Indeed, ectopic expression of FGF3 or FGF10 during mouse embryogenesis induces the formation of ectopic otic vesicles expressing some otic markers i.e., PAX2 [ ]. ..

    Mouse Assay:

    Article Title: Differential Requirement for Mesenchyme in the Proliferation and Maturation of Thymic Epithelial Progenitors
    Article Snippet: .. Moreover, thymus growth is retarded in mice lacking FGF-R2IIIb, a receptor for FGF7 and FGF10 , while FGF7 administration to mice following induction of graft-versus-host disease (GVHD) has a protective effect on thymic epithelium ( ). .. Moreover, FGF10-deficient mice display a hypoplastic thymus ( ).

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    R&D Systems recombinant mouse fgf10
    Effects of <t>FGF10</t> in organ culture. (A–H) Explants viewed at day 6. (A) Organ fed basal media only, with high power of the boxed area shown in (B). SM ( sm , arrowed) and epithelial ( e ) zones are indicated. (C,D) Organ fed with basal media supplemented with 5 ng/ml TGFβ1 has a cocoon‐like appearance. Interstitial zone indicated by asterisk. (E,F) Organ fed with basal media supplemented with 500 ng/ml FGF10. Note the apparent increased length versus organ fed basal media alone. (G,H) Organ fed with basal media supplemented with both 5 ng/ml TGFβ1 and 500 ng/ml FGF10. Cocooning is still apparent with prominent interstitial tissue (*) but the length of the tube appears increased versus the organ exposed to TGFβ1 alone. (I,J) Quantification of increases in urothelial tube length (I) and area (J) show that FGF10 ( n = 12) caused significant linear growth versus basal media alone ( n = 13). Addition of TGFβ1 ( n = 13) caused significant reduction in linear and area growth versus basal media alone. When FGF10 was added together with TGFβ1 ( n = 13) the negative effect of the latter on linear growth was overcome.
    Recombinant Mouse Fgf10, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant fgf10 protein
    (A) <t>FGF10</t> gene was targeted knocked-down from the LD605 cancer cell lines. (B) Co-cultured human stem cells were observed for the bladder cell markers with FGF10 knock-down cells. Left panel: RT-PCR results of UP III, CK8 and SMA were presented. Right
    Recombinant Fgf10 Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems fgf10
    Failed palate elevation associated with heightened tongue in mice overexpressing <t>Fgf10</t> in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened
    Fgf10, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 76 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effects of FGF10 in organ culture. (A–H) Explants viewed at day 6. (A) Organ fed basal media only, with high power of the boxed area shown in (B). SM ( sm , arrowed) and epithelial ( e ) zones are indicated. (C,D) Organ fed with basal media supplemented with 5 ng/ml TGFβ1 has a cocoon‐like appearance. Interstitial zone indicated by asterisk. (E,F) Organ fed with basal media supplemented with 500 ng/ml FGF10. Note the apparent increased length versus organ fed basal media alone. (G,H) Organ fed with basal media supplemented with both 5 ng/ml TGFβ1 and 500 ng/ml FGF10. Cocooning is still apparent with prominent interstitial tissue (*) but the length of the tube appears increased versus the organ exposed to TGFβ1 alone. (I,J) Quantification of increases in urothelial tube length (I) and area (J) show that FGF10 ( n = 12) caused significant linear growth versus basal media alone ( n = 13). Addition of TGFβ1 ( n = 13) caused significant reduction in linear and area growth versus basal media alone. When FGF10 was added together with TGFβ1 ( n = 13) the negative effect of the latter on linear growth was overcome.

    Journal: The Journal of Pathology

    Article Title: Overactivity or blockade of transforming growth factor‐β each generate a specific ureter malformation

    doi: 10.1002/path.5335

    Figure Lengend Snippet: Effects of FGF10 in organ culture. (A–H) Explants viewed at day 6. (A) Organ fed basal media only, with high power of the boxed area shown in (B). SM ( sm , arrowed) and epithelial ( e ) zones are indicated. (C,D) Organ fed with basal media supplemented with 5 ng/ml TGFβ1 has a cocoon‐like appearance. Interstitial zone indicated by asterisk. (E,F) Organ fed with basal media supplemented with 500 ng/ml FGF10. Note the apparent increased length versus organ fed basal media alone. (G,H) Organ fed with basal media supplemented with both 5 ng/ml TGFβ1 and 500 ng/ml FGF10. Cocooning is still apparent with prominent interstitial tissue (*) but the length of the tube appears increased versus the organ exposed to TGFβ1 alone. (I,J) Quantification of increases in urothelial tube length (I) and area (J) show that FGF10 ( n = 12) caused significant linear growth versus basal media alone ( n = 13). Addition of TGFβ1 ( n = 13) caused significant reduction in linear and area growth versus basal media alone. When FGF10 was added together with TGFβ1 ( n = 13) the negative effect of the latter on linear growth was overcome.

    Article Snippet: In some experiments the following were added: recombinant human TGFβ1 (240‐B; R & D Systems, Minneapolis, MN, USA); TGFβR inhibitor LY2109761 (A8464, Generon, Slough, UK); TGFβR inhibitor SB431542 (04‐0010; Generon); recombinant mouse FGF18 (CYT‐064; ProSpec, Ness‐Ziona, Israel); recombinant mouse FGF10 (6224‐FG‐025, R & D Systems); and 5‐bromo‐2′‐deoxyuridine (BrdU; B5002‐100MG, Sigma‐Aldrich), applied 2 h before harvest.

    Techniques: Organ Culture

    (A) FGF10 gene was targeted knocked-down from the LD605 cancer cell lines. (B) Co-cultured human stem cells were observed for the bladder cell markers with FGF10 knock-down cells. Left panel: RT-PCR results of UP III, CK8 and SMA were presented. Right

    Journal: In vitro cellular & developmental biology. Animal

    Article Title: Bladder cancer cell in co-culture induces human stem cell differentiation to urothelial cells through paracrine FGF10 signaling

    doi: 10.1007/s11626-013-9662-9

    Figure Lengend Snippet: (A) FGF10 gene was targeted knocked-down from the LD605 cancer cell lines. (B) Co-cultured human stem cells were observed for the bladder cell markers with FGF10 knock-down cells. Left panel: RT-PCR results of UP III, CK8 and SMA were presented. Right

    Article Snippet: Recombinant FGF10 protein (R & D Systems, Minneapolis, MN) was diluted from a stock containing hanks balanced salt solution and bovine serum albumin to a final media concentration of 50, 100, 150 and 200 ng/ml.

    Techniques: Cell Culture, Reverse Transcription Polymerase Chain Reaction

    (A) FGF10 overexpression in LD605. RT-PCR analysis was performed with total RNAs extracted from LD605, LD611 and A549 cancer cells. Total RNAs were extracted from HAFSC and lung adenocarcinoma A549 cells. SC stands for human stem cells, 605 stands for

    Journal: In vitro cellular & developmental biology. Animal

    Article Title: Bladder cancer cell in co-culture induces human stem cell differentiation to urothelial cells through paracrine FGF10 signaling

    doi: 10.1007/s11626-013-9662-9

    Figure Lengend Snippet: (A) FGF10 overexpression in LD605. RT-PCR analysis was performed with total RNAs extracted from LD605, LD611 and A549 cancer cells. Total RNAs were extracted from HAFSC and lung adenocarcinoma A549 cells. SC stands for human stem cells, 605 stands for

    Article Snippet: Recombinant FGF10 protein (R & D Systems, Minneapolis, MN) was diluted from a stock containing hanks balanced salt solution and bovine serum albumin to a final media concentration of 50, 100, 150 and 200 ng/ml.

    Techniques: Over Expression, Reverse Transcription Polymerase Chain Reaction

    Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened

    Journal: The Journal of Biological Chemistry

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    doi: 10.1074/jbc.M112.432286

    Figure Lengend Snippet: Failed palate elevation associated with heightened tongue in mice overexpressing Fgf10 in the tongue. A–E , comparison of tongue height through mid-level of tongues of E14.5 control ( A and C ) and Wnt1-Cre ; pMes-Fgf10 ( B and D ) mice reveals a heightened

    Article Snippet: We then determined whether inactivation of Tak1 could lead to overexpression of FGF10 in the CNC-derived mesenchymal cells in the developing tongue by in situ hybridization and immunohistochemical staining.

    Techniques: Mouse Assay

    Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions

    Journal: The Journal of Biological Chemistry

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    doi: 10.1074/jbc.M112.432286

    Figure Lengend Snippet: Enhanced cell proliferation in the tongue of Wnt1-Cre ; Tak1 F/F mice is associated with overexpression of Fgf10 . A and B , BrdU labeling in the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F embryo ( B ). BrdU-positive cells within the two arbitrary regions

    Article Snippet: We then determined whether inactivation of Tak1 could lead to overexpression of FGF10 in the CNC-derived mesenchymal cells in the developing tongue by in situ hybridization and immunohistochemical staining.

    Techniques: Mouse Assay, Over Expression, Labeling

    Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in

    Journal: The Journal of Biological Chemistry

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    doi: 10.1074/jbc.M112.432286

    Figure Lengend Snippet: Inhibition of p38 MAPK promotes Fgf10 expression in primary tongue mesenchymal cells. A and B , immunostaining on the tongue of E13.5 control ( A ) and Wnt1-Cre ; Tak1 F/F mutant ( B ) reveals a significantly reduced level of phosphorylated p38 MAPK ( p -p38) in

    Article Snippet: We then determined whether inactivation of Tak1 could lead to overexpression of FGF10 in the CNC-derived mesenchymal cells in the developing tongue by in situ hybridization and immunohistochemical staining.

    Techniques: Inhibition, Expressing, Immunostaining, Mutagenesis

    FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation

    Journal: The Journal of Biological Chemistry

    Article Title: Mice with Tak1 Deficiency in Neural Crest Lineage Exhibit Cleft Palate Associated with Abnormal Tongue Development *

    doi: 10.1074/jbc.M112.432286

    Figure Lengend Snippet: FGF10 stimulates tongue cell proliferation in organ culture. A and B , BrdU labeling shows FGF10 significantly stimulates cell proliferation in E13.5 wild type tongue compared with BSA control. C–G , BrdU labeling shows inhibition of cell proliferation

    Article Snippet: We then determined whether inactivation of Tak1 could lead to overexpression of FGF10 in the CNC-derived mesenchymal cells in the developing tongue by in situ hybridization and immunohistochemical staining.

    Techniques: Organ Culture, Labeling, Inhibition

    Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Journal: Development (Cambridge, England)

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    doi: 10.1242/dev.079236

    Figure Lengend Snippet: Fgf10-induced lacrimal gland budding was abolished in the Ugdh mutants. ( A-F ) In E13.5 control explant culture, BSA-containing beads did not perturb budding of the endogenous lacrimal gland (A, arrow), whereas Fgf10-containing beads induced ectopic lacrimal

    Article Snippet: We reasoned that excessive dispersion of Fgf10 in Ugdh mutant mesenchyme would probably lower its local concentration, effectively reducing the inductive strength of Fgf10 in promoting lacrimal gland budding.

    Techniques:

    Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Journal: Development (Cambridge, England)

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    doi: 10.1242/dev.079236

    Figure Lengend Snippet: Ugdh deletion abolished GAG synthesis. ( A-H ) At E10.5, the Ugdh CKO mutants lost CS and HS (3G10) staining in the mesenchyme (A,B,E,F, arrows). There was little HS 10E4 staining in the mesenchyme at this stage (C,G), but the LACE staining of Fgf10/Fgfr2b,

    Article Snippet: We reasoned that excessive dispersion of Fgf10 in Ugdh mutant mesenchyme would probably lower its local concentration, effectively reducing the inductive strength of Fgf10 in promoting lacrimal gland budding.

    Techniques: Staining

    The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Journal: Development (Cambridge, England)

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    doi: 10.1242/dev.079236

    Figure Lengend Snippet: The Ugdh mutants preserved the mesenchymal Fgf10 expression but lost the epithelial FGF signaling in lacrimal gland development. ( A-J ) RNA in situ hybridization showed that the periocular markers Crabp1, FoxC1 and Pitx2 were unaffected in E10.5 and E12.5

    Article Snippet: We reasoned that excessive dispersion of Fgf10 in Ugdh mutant mesenchyme would probably lower its local concentration, effectively reducing the inductive strength of Fgf10 in promoting lacrimal gland budding.

    Techniques: Expressing, RNA In Situ Hybridization

    Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Journal: Development (Cambridge, England)

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    doi: 10.1242/dev.079236

    Figure Lengend Snippet: Expanded Fgf10 diffusion in the Ugdh mutants. ( A , B ) Western blots of E13.5 periocular mesenchyme showed that the Fgf10 protein was expressed at similar levels in control and Ugdh CKO mutants. After normalization using ERK proteins in the same lysates,

    Article Snippet: We reasoned that excessive dispersion of Fgf10 in Ugdh mutant mesenchyme would probably lower its local concentration, effectively reducing the inductive strength of Fgf10 in promoting lacrimal gland budding.

    Techniques: Diffusion-based Assay, Western Blot

    Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Journal: Development (Cambridge, England)

    Article Title: Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development

    doi: 10.1242/dev.079236

    Figure Lengend Snippet: Mesenchymal ablation of Ndst1/2 , but not Hs6st/Hs2st , disrupted lacrimal gland budding. ( A-H ) Mesenchymal deletion of Ndst1 ( Wnt1-Cre; Ndst1 flox/flox or Ndst1 CKO ) disrupted both HS 10E4 staining and the Fgf10/Fgfr2b LACE signal, but lacrimal gland budding

    Article Snippet: We reasoned that excessive dispersion of Fgf10 in Ugdh mutant mesenchyme would probably lower its local concentration, effectively reducing the inductive strength of Fgf10 in promoting lacrimal gland budding.

    Techniques: Staining