rabbit stub1 polyclonal  (Proteintech)

 
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    Name:
    Rabbit STUB1 Polyclonal
    Description:
    The STUB1 antibody from Proteintech is a rabbit polyclonal antibody to a peptide of human STUB1 This antibody recognizes human mouse rat antigen The STUB1 antibody has been validated for the following applications ELISA IF IHC WB analysis
    Catalog Number:
    55430-1-AP
    Price:
    [321.93]
    Applications:
    IHC,Western Blot,ELISA,Immunofluorescence
    Host:
    Rabbit
    Conjugate:
    Unconjugated
    Immunogen:
    Peptide
    Size:
    150 ul
    Category:
    Antibody
    Antibody Type:
    Primary antibody
    Isotype:
    IgG
    Reactivity:
    Human Mouse Rat
    Buy from Supplier


    Structured Review

    Proteintech rabbit stub1 polyclonal
    The STUB1 antibody from Proteintech is a rabbit polyclonal antibody to a peptide of human STUB1 This antibody recognizes human mouse rat antigen The STUB1 antibody has been validated for the following applications ELISA IF IHC WB analysis
    https://www.bioz.com/result/rabbit stub1 polyclonal/product/Proteintech
    Average 92 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    rabbit stub1 polyclonal - by Bioz Stars, 2020-09
    92/100 stars

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    Chromatin Immunoprecipitation:

    Article Title: Anisomycin prevents OGD-induced necroptosis by regulating the E3 ligase CHIP
    Article Snippet: .. The antibody against β-actin (T4026) was from Sigma-Aldrich, the antibody JNK (mAb#4668) was from Cell Signaling Technology (CST, Beverly, MA, USA), The antibody against CHIP (55430-1-AP) was from Proteintech (WuHan, China), anisomycin (HY-18982) and the JNK inhibitor SP600125 (HY-12041) were from MCE (Monmouth Junction, NJ, USA) and AnnexinV-FITC Apoptosis Detection Kit was from Vazyme (Nanjing, China). .. The wild-type CHIP (pcDNA3.1-CHIP) was obtained from Addgene (Cambridge, MA, USA), the vector pcDNA3.1, mutants of CHIP in pcDNA-3.1-K30A/T246M, PGPU6-GFP -shNC, and PGPU6-GFP-sh-CHIP were all constructed by GenePharma (Shanghai, China).

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  • 96
    Proteintech rabbit anti six2
    Gene expression changes in the <t>Six2</t> GCE/+ kidney. A) Genes differentially expressed (DE) at ≤−0.4 or ≥0.4 LogFC of Six2 +/+ values at 15.5dpc in Six2 GCE/+ and ≤−1 or ≥1 LogFC of wildtype in 11.5 dpc Six2 GCE/GCE ; adjusted p
    Rabbit Anti Six2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti six2/product/Proteintech
    Average 96 stars, based on 27 article reviews
    Price from $9.99 to $1999.99
    rabbit anti six2 - by Bioz Stars, 2020-09
    96/100 stars
      Buy from Supplier

    98
    Proteintech rabbit anti prox1
    ILK controls lymphatic vascular growth and VEGFR3 tyrosine phosphorylation in adult mice LSM images of a whole‐mount stained adult <t>Prox1‐Cre</t> ERT2 ;Ilk +/+ mouse ear (referred to as “adult control”) and Prox1‐Cre ERT2 ;Ilk ∆/∆ mouse ear (referred to as “adult ILK K.O.”), with higher magnification images indicated by dashed lines. Scale bars: 500 and 100 μm, respectively. LSM images of a whole‐mount stained adult control and ILK K.O. ear, with higher magnification images indicated by dashed lines. Arrows point to proliferating LECs. Scale bars: 100 and 20 μm, respectively. Dermal lymph vessel density as determined by VEGFR3‐positive area normalised to the total analysed area of adult control or ILK K.O. mice ( n = 4 control and n = 5 ILK K.O. mice), * P = 0.025. LEC proliferation as determined by phospho‐Histone H3‐positive LECs normalised to analysed VEGFR3‐positive area in the skin of adult control or ILK K.O. mice ( n = 7 control and n = 5 ILK K.O. mice), * P = 0.004. VEGFR3 tyrosine phosphorylation as determined by ELISA of skin lysates of adult control or ILK K.O. mice ( n = 3 mice per genotype), P = 0.062. LSM images of a whole‐mount stained adult control and ILK K.O. cornea, with detailed images on their right (L′, M′). Arrows point to lymph vessels protruding into the cornea (encircled by a dotted line). Scale bars: 500 μm and 100 μm, respectively. Number of lymph vessels in control or ILK K.O. corneas ( n = 5 and n = 7 corneas), * P = 0.02. Data information: Data are presented as means ± SEM, shown as percentage of control mice, unpaired two‐tailed Student's t ‐test.
    Rabbit Anti Prox1, supplied by Proteintech, used in various techniques. Bioz Stars score: 98/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti prox1/product/Proteintech
    Average 98 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    rabbit anti prox1 - by Bioz Stars, 2020-09
    98/100 stars
      Buy from Supplier

    Image Search Results


    Gene expression changes in the Six2 GCE/+ kidney. A) Genes differentially expressed (DE) at ≤−0.4 or ≥0.4 LogFC of Six2 +/+ values at 15.5dpc in Six2 GCE/+ and ≤−1 or ≥1 LogFC of wildtype in 11.5 dpc Six2 GCE/GCE ; adjusted p

    Journal: Kidney international

    Article Title: Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number.

    doi: 10.1016/j.kint.2017.09.015

    Figure Lengend Snippet: Gene expression changes in the Six2 GCE/+ kidney. A) Genes differentially expressed (DE) at ≤−0.4 or ≥0.4 LogFC of Six2 +/+ values at 15.5dpc in Six2 GCE/+ and ≤−1 or ≥1 LogFC of wildtype in 11.5 dpc Six2 GCE/GCE ; adjusted p

    Article Snippet: The following primary antibodies were used: mouse anti-calbindin D28K (Sigma-Aldrich C9848), mouse anti-cytokeratin (Abcam Ab11213 and ), rabbit anti-SIX2 (Proteintech 11562–1-AP), rabbit anti-JAG1 (Abcam ab7771), mouse anti-SIX2 (Abnova H00010736-MO1), rat anti-Ecad (Invitrogen 13–1900).

    Techniques: Expressing

    Analysis of transcriptional changes A) Unsupervised clustering of the top 250 differentially expressed genes between 11.5 dpc Six2 GCE/GCE and Six2 +/+ . Each row represents a gene, each column an independent sample. Colour indicates normalised expression (Z-score) blue is low, red high. B) Gene set testing reveals an upregulation of pathways associated with growth (MYC targets V1 and V2), progenitor maintenance (mTOR, mTORC1 signalling), and differentiation (PI3K signalling) in Six2 GCE/+ . The pathways associated with MYC and mTORC1 are downregulated in Six2 GCE/GCE . D ) MYC protein levels are significantly increased in the Six2 GCE/+ . Points represent average values from three independent litters. Unpaired t test.

    Journal: Kidney international

    Article Title: Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number.

    doi: 10.1016/j.kint.2017.09.015

    Figure Lengend Snippet: Analysis of transcriptional changes A) Unsupervised clustering of the top 250 differentially expressed genes between 11.5 dpc Six2 GCE/GCE and Six2 +/+ . Each row represents a gene, each column an independent sample. Colour indicates normalised expression (Z-score) blue is low, red high. B) Gene set testing reveals an upregulation of pathways associated with growth (MYC targets V1 and V2), progenitor maintenance (mTOR, mTORC1 signalling), and differentiation (PI3K signalling) in Six2 GCE/+ . The pathways associated with MYC and mTORC1 are downregulated in Six2 GCE/GCE . D ) MYC protein levels are significantly increased in the Six2 GCE/+ . Points represent average values from three independent litters. Unpaired t test.

    Article Snippet: The following primary antibodies were used: mouse anti-calbindin D28K (Sigma-Aldrich C9848), mouse anti-cytokeratin (Abcam Ab11213 and ), rabbit anti-SIX2 (Proteintech 11562–1-AP), rabbit anti-JAG1 (Abcam ab7771), mouse anti-SIX2 (Abnova H00010736-MO1), rat anti-Ecad (Invitrogen 13–1900).

    Techniques: Expressing

    Validation of haploinsufficiency and compromised progenitor state A ) Six2 mRNA is reduced by 50% in Six2 GCE/+ compared to Six2 +/+ at 15.5 dpc. Data is the average of three biological replicates from each genotype, p=0.0003. mRNA levels expressed relative to Six2 +/+ . B for full gels. C ) Densitometry analysis showing reduced SIX2 relative to GAPDH (p=0.014), no change in PAX2 relative to GAPDH (p=0.256), reduced SIX2 relative to PAX2 (p=0.049). Data represents the average of 4 biological replicates. D E ) Pseudocoloured map of SIX2 intensity in representative Six2 +/+ and Six2 GCE/+ samples imaged and displayed on the same settings. Colour scale indicates fluorescence intensity units. Scale bar 100μm. F ) Box and whisker plot of mean SIX2 intensity per cap cluster for Six2 +/+ (n=104) vs Six2 GCE/+ (n=55), two sample t-test with welch’s correction p=6.4e-10. G) Cited1 mRNA levels are dramatically reduced in the Six2 GCE/+ compared to Six2 +/+ (p=0.00005). Error bars on all graphs represent SEM, p values from two-tailed t-tests with Welch’s correction.

    Journal: Kidney international

    Article Title: Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number.

    doi: 10.1016/j.kint.2017.09.015

    Figure Lengend Snippet: Validation of haploinsufficiency and compromised progenitor state A ) Six2 mRNA is reduced by 50% in Six2 GCE/+ compared to Six2 +/+ at 15.5 dpc. Data is the average of three biological replicates from each genotype, p=0.0003. mRNA levels expressed relative to Six2 +/+ . B for full gels. C ) Densitometry analysis showing reduced SIX2 relative to GAPDH (p=0.014), no change in PAX2 relative to GAPDH (p=0.256), reduced SIX2 relative to PAX2 (p=0.049). Data represents the average of 4 biological replicates. D E ) Pseudocoloured map of SIX2 intensity in representative Six2 +/+ and Six2 GCE/+ samples imaged and displayed on the same settings. Colour scale indicates fluorescence intensity units. Scale bar 100μm. F ) Box and whisker plot of mean SIX2 intensity per cap cluster for Six2 +/+ (n=104) vs Six2 GCE/+ (n=55), two sample t-test with welch’s correction p=6.4e-10. G) Cited1 mRNA levels are dramatically reduced in the Six2 GCE/+ compared to Six2 +/+ (p=0.00005). Error bars on all graphs represent SEM, p values from two-tailed t-tests with Welch’s correction.

    Article Snippet: The following primary antibodies were used: mouse anti-calbindin D28K (Sigma-Aldrich C9848), mouse anti-cytokeratin (Abcam Ab11213 and ), rabbit anti-SIX2 (Proteintech 11562–1-AP), rabbit anti-JAG1 (Abcam ab7771), mouse anti-SIX2 (Abnova H00010736-MO1), rat anti-Ecad (Invitrogen 13–1900).

    Techniques: Fluorescence, Whisker Assay, Two Tailed Test

    Cap mesenchyme lacking one copy of Six2 undergoes premature differentiation in the absence of Fgf20 . A) Staining of the CM (SIX2, red), ureteric tree (ECAD, green), and nuclei (DAPI, blue) in a 15.5 dpc Six2 +/+ Fgf20 −/− kidney. Scale 200μm. B) Nephron progenitors exhaust before 15.5 dpc in Six2 GCE/+ Fgf20 −/− kidneys. Dilated nephrons are observed (arrows) and the ureteric tree is underdeveloped. Staining and scale as per A. C) Maximum intensity projection of the CM (SIX2, green), tree (ECAD, grey), renal vesicles (JAG1, red), and nuclei (DAPI, blue) in a 12.5 dpc Six2 +/+ Fgf20 +/− kidney, scale 50μm. D) Rendering of the tree (grey) and renal vesicles (red) from C, scale 50μm. E) Zoom of boxed region in E shows t-stage tip with two renal vesicles attached on medullary side, scale 20μm. F) 12.5 dpc Six2 GCE/+ Fgf20 −/− kidney as per C, scale 50μm. G) Rendering from F, scale 50μm. H) Zoom of region in G showing t-stage tip with 5 renal vesicles, 2 in ectopic positions, scale 20μm.

    Journal: Kidney international

    Article Title: Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number.

    doi: 10.1016/j.kint.2017.09.015

    Figure Lengend Snippet: Cap mesenchyme lacking one copy of Six2 undergoes premature differentiation in the absence of Fgf20 . A) Staining of the CM (SIX2, red), ureteric tree (ECAD, green), and nuclei (DAPI, blue) in a 15.5 dpc Six2 +/+ Fgf20 −/− kidney. Scale 200μm. B) Nephron progenitors exhaust before 15.5 dpc in Six2 GCE/+ Fgf20 −/− kidneys. Dilated nephrons are observed (arrows) and the ureteric tree is underdeveloped. Staining and scale as per A. C) Maximum intensity projection of the CM (SIX2, green), tree (ECAD, grey), renal vesicles (JAG1, red), and nuclei (DAPI, blue) in a 12.5 dpc Six2 +/+ Fgf20 +/− kidney, scale 50μm. D) Rendering of the tree (grey) and renal vesicles (red) from C, scale 50μm. E) Zoom of boxed region in E shows t-stage tip with two renal vesicles attached on medullary side, scale 20μm. F) 12.5 dpc Six2 GCE/+ Fgf20 −/− kidney as per C, scale 50μm. G) Rendering from F, scale 50μm. H) Zoom of region in G showing t-stage tip with 5 renal vesicles, 2 in ectopic positions, scale 20μm.

    Article Snippet: The following primary antibodies were used: mouse anti-calbindin D28K (Sigma-Aldrich C9848), mouse anti-cytokeratin (Abcam Ab11213 and ), rabbit anti-SIX2 (Proteintech 11562–1-AP), rabbit anti-JAG1 (Abcam ab7771), mouse anti-SIX2 (Abnova H00010736-MO1), rat anti-Ecad (Invitrogen 13–1900).

    Techniques: Staining

    Increased branching, tip proliferation, and nephron endowment in Six2 GCE/+ . A ) Whole organ OPT of SIX2-antibody stained Six2 +/+ and Six2 GCE/+ kidneys at 15.5 dpc, 19.5 dpc, and P2. Scale 300μm for all. Exposures were optimised for each sample hence signal intensity should not be compared between images. B ) Niche counts from OPT data for 15.5 dpc (n = 9 Six2 +/+ , 8 Six2 GCE/+ ), 19.5 dpc (n = 8 Six2 +/+ , 8 Six2 GCE/+ ), and P2 (n = 8 Six2 +/+ , 9 Six2 GCE/+ ). C ) Max. intensity projection confocal data from 15.5 dpc and 19.5 dpc Six2 +/+ and Six2 GCE/+ kidneys stained with SIX2 (red) and CYTOK (white). Scale bars 30μm. Exposures were optimised for each sample hence signal intensity should not be compared between images. D ) Tip and cap cell number at 15.5 dpc. Each data point represents average cell number per niche in an individual sample; Sample numbers = 9 Six2 +/+ , 8 Six2 GCE/+ . E ) Tip and cap cell number at 19.5 dpc. Points as per D, n= 9 Six2 +/+ , 8 Six2 GCE/+ . F ) % EdU incorporation for tip and cap cell populations at 13.5 dpc, 30 minutes after exposure to EdU. Each data point represents % incorporation per sample, data derives from three replicate experiments; n = 8 Six2 +/+ , 9 Six2 GCE/+ . G ) Comparison of estimated glomerular number between P21 (adult) Six2 +/+ and Six2 GCE/+ by stereology; n= 10 Six2 +/+ , 12 Six2 GCE/+ . Error bars in all graphs represent SEM, p values determined by 1-tailed t-test with Welch’s correction.

    Journal: Kidney international

    Article Title: Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number.

    doi: 10.1016/j.kint.2017.09.015

    Figure Lengend Snippet: Increased branching, tip proliferation, and nephron endowment in Six2 GCE/+ . A ) Whole organ OPT of SIX2-antibody stained Six2 +/+ and Six2 GCE/+ kidneys at 15.5 dpc, 19.5 dpc, and P2. Scale 300μm for all. Exposures were optimised for each sample hence signal intensity should not be compared between images. B ) Niche counts from OPT data for 15.5 dpc (n = 9 Six2 +/+ , 8 Six2 GCE/+ ), 19.5 dpc (n = 8 Six2 +/+ , 8 Six2 GCE/+ ), and P2 (n = 8 Six2 +/+ , 9 Six2 GCE/+ ). C ) Max. intensity projection confocal data from 15.5 dpc and 19.5 dpc Six2 +/+ and Six2 GCE/+ kidneys stained with SIX2 (red) and CYTOK (white). Scale bars 30μm. Exposures were optimised for each sample hence signal intensity should not be compared between images. D ) Tip and cap cell number at 15.5 dpc. Each data point represents average cell number per niche in an individual sample; Sample numbers = 9 Six2 +/+ , 8 Six2 GCE/+ . E ) Tip and cap cell number at 19.5 dpc. Points as per D, n= 9 Six2 +/+ , 8 Six2 GCE/+ . F ) % EdU incorporation for tip and cap cell populations at 13.5 dpc, 30 minutes after exposure to EdU. Each data point represents % incorporation per sample, data derives from three replicate experiments; n = 8 Six2 +/+ , 9 Six2 GCE/+ . G ) Comparison of estimated glomerular number between P21 (adult) Six2 +/+ and Six2 GCE/+ by stereology; n= 10 Six2 +/+ , 12 Six2 GCE/+ . Error bars in all graphs represent SEM, p values determined by 1-tailed t-test with Welch’s correction.

    Article Snippet: The following primary antibodies were used: mouse anti-calbindin D28K (Sigma-Aldrich C9848), mouse anti-cytokeratin (Abcam Ab11213 and ), rabbit anti-SIX2 (Proteintech 11562–1-AP), rabbit anti-JAG1 (Abcam ab7771), mouse anti-SIX2 (Abnova H00010736-MO1), rat anti-Ecad (Invitrogen 13–1900).

    Techniques: Staining

    Analysis of vascular heterogeneity development. a Pseudotime trajectory of vascular differentiation in the kidney. VP, vascular progenitor; PTC, peritubular capillary; AA/LA, afferent arteriole/large arteries (pre-glomerular); AVR/V, ascending vasa recta/venous blood vessels; EA, efferent arteriole; GC, glomerular capillaries; DVR, descending vasa recta. b Heat maps denoting genes that become differentially expressed as pre-glomerular arteries branch from vascular progenitor cells. Notable genes of venous peritubular progenitor capillaries ( Cryab , Igfbp5 , Plvap ) and arteries ( Jag1 , Fbln5 , Gja5 ) are shown on the right. c Heat maps denoting genes that become differentially expressed as glomerular capillaries (GC) and postglomerular arteries branch from embryonic progenitor capillaries which mature into peritubular capillaries. Notable genes of glomerular capillaries ( Sema5a , Lpl ), postglomerular arteries ( Aqp1 , Slc14a1 ), and peritubular capillaries ( Igfbp5 , Plvap ) are on the right. d – g Pseudo-time trajectory plots denoting the expression of genes enriched in particular vascular clusters. Plots include Aplnr in vascular progenitor cells (VP) ( d ), Plvap in veins (V), VPs, and peritubular capillaries (PTC)( e ), Sox17 in afferent arterioles/large pre-glomerular arteries (AA/LA) and descending vasa recta/efferent arterioles (DVR/EA)( f ), and Lpl in glomerular capillaries (GC)( g ). h Immunofluorescent staining of the apelin receptor ( Aplnr ) in E17 kidney. Endothelial cells were stained with endomucin ( Emcn ). SSB, s-shaped body; VP, vascular progenitor; Angio., angiogenic vessel; GC, glomerular capillary; V, vein; A, arteriole. Scale bars: first panel 40 μm, second panel 5 μm, third and fourth panel 10 μm. i Pie chart denoting mean fluorescent intensity of Aplnr antibody staining in peritibular capillaries, veins, arteries, and glomerular capillaries. n = 3, average of 5 frames of view. j R26R-Confetti E18 mouse kidneys cut in half sagittally after tamoxifen induction at E11. GC, glomerular capillary; PTC, peritubular capillary. Scale bars: first panel 100 μm, second to sixth panel 5 μm. k Bar graph denoting the number of fluorescent reporters found in identified vascular structures. n > 10 for each structure. Art, Arteries; VR, Vasa Recta. l E13 mouse kidney showing the primary vascular plexus exists as generic capillaries (the vascular progenitor cells) before subvascular specification at E14-E15 stages. Dotted lines outline the cortex and medulla. Endothelial cells are stained with endomucin ( Emcn ) and the outer cortex of the kidney is denoted by Six2 staining of nephron progenitors. Scale bar 100 μm.

    Journal: Nature Communications

    Article Title: Molecular determinants of nephron vascular specialization in the kidney

    doi: 10.1038/s41467-019-12872-5

    Figure Lengend Snippet: Analysis of vascular heterogeneity development. a Pseudotime trajectory of vascular differentiation in the kidney. VP, vascular progenitor; PTC, peritubular capillary; AA/LA, afferent arteriole/large arteries (pre-glomerular); AVR/V, ascending vasa recta/venous blood vessels; EA, efferent arteriole; GC, glomerular capillaries; DVR, descending vasa recta. b Heat maps denoting genes that become differentially expressed as pre-glomerular arteries branch from vascular progenitor cells. Notable genes of venous peritubular progenitor capillaries ( Cryab , Igfbp5 , Plvap ) and arteries ( Jag1 , Fbln5 , Gja5 ) are shown on the right. c Heat maps denoting genes that become differentially expressed as glomerular capillaries (GC) and postglomerular arteries branch from embryonic progenitor capillaries which mature into peritubular capillaries. Notable genes of glomerular capillaries ( Sema5a , Lpl ), postglomerular arteries ( Aqp1 , Slc14a1 ), and peritubular capillaries ( Igfbp5 , Plvap ) are on the right. d – g Pseudo-time trajectory plots denoting the expression of genes enriched in particular vascular clusters. Plots include Aplnr in vascular progenitor cells (VP) ( d ), Plvap in veins (V), VPs, and peritubular capillaries (PTC)( e ), Sox17 in afferent arterioles/large pre-glomerular arteries (AA/LA) and descending vasa recta/efferent arterioles (DVR/EA)( f ), and Lpl in glomerular capillaries (GC)( g ). h Immunofluorescent staining of the apelin receptor ( Aplnr ) in E17 kidney. Endothelial cells were stained with endomucin ( Emcn ). SSB, s-shaped body; VP, vascular progenitor; Angio., angiogenic vessel; GC, glomerular capillary; V, vein; A, arteriole. Scale bars: first panel 40 μm, second panel 5 μm, third and fourth panel 10 μm. i Pie chart denoting mean fluorescent intensity of Aplnr antibody staining in peritibular capillaries, veins, arteries, and glomerular capillaries. n = 3, average of 5 frames of view. j R26R-Confetti E18 mouse kidneys cut in half sagittally after tamoxifen induction at E11. GC, glomerular capillary; PTC, peritubular capillary. Scale bars: first panel 100 μm, second to sixth panel 5 μm. k Bar graph denoting the number of fluorescent reporters found in identified vascular structures. n > 10 for each structure. Art, Arteries; VR, Vasa Recta. l E13 mouse kidney showing the primary vascular plexus exists as generic capillaries (the vascular progenitor cells) before subvascular specification at E14-E15 stages. Dotted lines outline the cortex and medulla. Endothelial cells are stained with endomucin ( Emcn ) and the outer cortex of the kidney is denoted by Six2 staining of nephron progenitors. Scale bar 100 μm.

    Article Snippet: The following antibodies were used: chicken anti-GFP (for Flk-GFP; Aves, GFP-1020, 1:500), goat anti-Cx40/Gja5 (Santa Cruz, sc-20466, 1:100), rabbit anti-Collagen IV (Millipore, AB756P, 1:400), goat anti-Nrp1 (R & D Systems, AF566, 1:100), rat anti-Plvap (BD Pharmingen, 550563, 1:100), goat anti-Sox17 (R & D Systems, AF1924, 1:100), rat anti-Endomucin (Santa Cruz, sc-65495, 1:100), rabbit anti-Aquaporin1 (Biorad, MCA2100, 1:100), rabbit anti-Tbx3 (Abcam, ab99302, 1:100), rabbit anti-Aplnr (Protein Tech, 20341–1-AP, 1:100), goat anti-Igfbp5 (R & D Systems, AF578, 1:100), goat anti-Igfbp7 (Abcam, ab129302, 1:100), rabbit anti-Six2 (Protein Tech, 11562–1-AP, 1:100).

    Techniques: Expressing, Staining

    RIG-I-Like signaling and apoptosis are increased in kidneys of Six2 Cre Dnmt1 f/f mice. (A) The GSEA enrichment plots of RNA sequencing data showing enrichment for RIG-I–like signaling in Six2 Cre Dnmt1 f/f mice. (B) Relative expression level of genes involved in RIG-I–like signaling. y -axis is normalized expression level determined by RNA sequencing. Asterisks represent significant differences calculated by DESeq2. (C) The GSEA enrichment plots of RNA sequencing data of P53 signaling in Six2 Cre Dnmt1 f/f mice. (D) Relative expression level of genes involved in p53 signaling. y -axis is normalized expression level determined by RNA sequencing. Asterisks represent significant differences calculated by DESeq2. (E) Left panel: immunofluorescence staining of P53 (red) and TUNEL assay (red) in P0 Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice kidneys; right panel: quantification of P53- and TUNEL-positive signaling according to the staining. (F) Left panel: immunofluorescence staining of Ki67 (red) in P0 Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice kidneys; right panel: quantification of Ki67-positive cells. (G) Schematic of our model which Dnmt1 deletion in progeny of Six2 -positive cells affects kidney development. * P

    Journal: Journal of the American Society of Nephrology : JASN

    Article Title: DNMT1 in Six2 Progenitor Cells Is Essential for Transposable Element Silencing and Kidney Development

    doi: 10.1681/ASN.2018070687

    Figure Lengend Snippet: RIG-I-Like signaling and apoptosis are increased in kidneys of Six2 Cre Dnmt1 f/f mice. (A) The GSEA enrichment plots of RNA sequencing data showing enrichment for RIG-I–like signaling in Six2 Cre Dnmt1 f/f mice. (B) Relative expression level of genes involved in RIG-I–like signaling. y -axis is normalized expression level determined by RNA sequencing. Asterisks represent significant differences calculated by DESeq2. (C) The GSEA enrichment plots of RNA sequencing data of P53 signaling in Six2 Cre Dnmt1 f/f mice. (D) Relative expression level of genes involved in p53 signaling. y -axis is normalized expression level determined by RNA sequencing. Asterisks represent significant differences calculated by DESeq2. (E) Left panel: immunofluorescence staining of P53 (red) and TUNEL assay (red) in P0 Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice kidneys; right panel: quantification of P53- and TUNEL-positive signaling according to the staining. (F) Left panel: immunofluorescence staining of Ki67 (red) in P0 Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice kidneys; right panel: quantification of Ki67-positive cells. (G) Schematic of our model which Dnmt1 deletion in progeny of Six2 -positive cells affects kidney development. * P

    Article Snippet: Immunostaining were performed using the following primary antibodies: DNMT1 (ab188453; Abcam), SIX2 (11562–1-AP; Proteintech), p-53 (#2526; CST), fluorescein labeled Peanut agglutinin (PNA), Lotus tetragonolobus lectin (LTL), and Dolichos biflorus agglutinin (DBA) (FL-1071, FL-1321, FL-1031; Vector) after heat-induced antigen retrieval by Tris-EDTA buffer (pH 9.0 or 6.0).

    Techniques: Mouse Assay, RNA Sequencing Assay, Expressing, Immunofluorescence, Staining, TUNEL Assay

    Dnmt1 loss results in broad cytosine methylation changes. (A) RRBS and RNA sequencing analysis of kidneys of Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. (B) Global CpG methylation in Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys. (C) Methylation distributions of CpGs in Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys. Histogram plots showing counts by CpG methylation level ( x -axis: 0%–100%) distributed across 20 bins of 5% intervals. (D) Annotation of DMRs by kidney-specific chromatin states. (E) Gene ontology annotation analysis for the DMRs between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys. (F) Distribution of DMRs in different genomic elements. Blue bar represents DMRs detected between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. Orange bar represents DMRs detected between Dnmt1 f/f P0 and wild-type adult mice. (G) Distribution of DMRs in different transposable elements. (H) Relative expression level of Duxf3 ( Dux ). y -axis is normalized expression level determined by RNA sequencing. Asterisks represent significant differences calculated by DESeq2. * P

    Journal: Journal of the American Society of Nephrology : JASN

    Article Title: DNMT1 in Six2 Progenitor Cells Is Essential for Transposable Element Silencing and Kidney Development

    doi: 10.1681/ASN.2018070687

    Figure Lengend Snippet: Dnmt1 loss results in broad cytosine methylation changes. (A) RRBS and RNA sequencing analysis of kidneys of Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. (B) Global CpG methylation in Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys. (C) Methylation distributions of CpGs in Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys. Histogram plots showing counts by CpG methylation level ( x -axis: 0%–100%) distributed across 20 bins of 5% intervals. (D) Annotation of DMRs by kidney-specific chromatin states. (E) Gene ontology annotation analysis for the DMRs between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys. (F) Distribution of DMRs in different genomic elements. Blue bar represents DMRs detected between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. Orange bar represents DMRs detected between Dnmt1 f/f P0 and wild-type adult mice. (G) Distribution of DMRs in different transposable elements. (H) Relative expression level of Duxf3 ( Dux ). y -axis is normalized expression level determined by RNA sequencing. Asterisks represent significant differences calculated by DESeq2. * P

    Article Snippet: Immunostaining were performed using the following primary antibodies: DNMT1 (ab188453; Abcam), SIX2 (11562–1-AP; Proteintech), p-53 (#2526; CST), fluorescein labeled Peanut agglutinin (PNA), Lotus tetragonolobus lectin (LTL), and Dolichos biflorus agglutinin (DBA) (FL-1071, FL-1321, FL-1031; Vector) after heat-induced antigen retrieval by Tris-EDTA buffer (pH 9.0 or 6.0).

    Techniques: Methylation, RNA Sequencing Assay, Mouse Assay, CpG Methylation Assay, Expressing

    Dnmt1 is critical for kidney development. (A) Expression of Dnmt1 , Dnmt3a , Dnmt3b , Tet1 , Tet2 , and Tet3 in Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys (P0) as analyzed by RNA sequencing. Asterisks represent FDR significant differences calculated by DESeq2. ** P

    Journal: Journal of the American Society of Nephrology : JASN

    Article Title: DNMT1 in Six2 Progenitor Cells Is Essential for Transposable Element Silencing and Kidney Development

    doi: 10.1681/ASN.2018070687

    Figure Lengend Snippet: Dnmt1 is critical for kidney development. (A) Expression of Dnmt1 , Dnmt3a , Dnmt3b , Tet1 , Tet2 , and Tet3 in Dnmt1 f/f and Six2 Cre Dnmt1 f/f mouse kidneys (P0) as analyzed by RNA sequencing. Asterisks represent FDR significant differences calculated by DESeq2. ** P

    Article Snippet: Immunostaining were performed using the following primary antibodies: DNMT1 (ab188453; Abcam), SIX2 (11562–1-AP; Proteintech), p-53 (#2526; CST), fluorescein labeled Peanut agglutinin (PNA), Lotus tetragonolobus lectin (LTL), and Dolichos biflorus agglutinin (DBA) (FL-1071, FL-1321, FL-1031; Vector) after heat-induced antigen retrieval by Tris-EDTA buffer (pH 9.0 or 6.0).

    Techniques: Expressing, RNA Sequencing Assay

    Dnmt1 is indispensable for renal epithelial cell differentiation. (A) Representative flow cytometry images of GFP-positive cells in Six2 Cre and Six2 Cre Dnmt1 f/f kidneys. (B) Quantification of GFP-positive cells. (C and D) Expression of Six2 and Cited1 in Dnmt1 f/f P0, Six2 Cre Dnmt1 f/f P0, and wild-type adult kidneys, as analyzed by qRT-PCR. (E) Heatmap of the DEGs between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. Color scheme uses z-score distribution. (F) Functional annotation analysis (DAVID) of the differentially expressed (up- and downregulated) genes. (G) Log 2 fold change of expression genes involved in kidney development. Asterisks represent FDR significant differences calculated by DESeq2. * P

    Journal: Journal of the American Society of Nephrology : JASN

    Article Title: DNMT1 in Six2 Progenitor Cells Is Essential for Transposable Element Silencing and Kidney Development

    doi: 10.1681/ASN.2018070687

    Figure Lengend Snippet: Dnmt1 is indispensable for renal epithelial cell differentiation. (A) Representative flow cytometry images of GFP-positive cells in Six2 Cre and Six2 Cre Dnmt1 f/f kidneys. (B) Quantification of GFP-positive cells. (C and D) Expression of Six2 and Cited1 in Dnmt1 f/f P0, Six2 Cre Dnmt1 f/f P0, and wild-type adult kidneys, as analyzed by qRT-PCR. (E) Heatmap of the DEGs between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. Color scheme uses z-score distribution. (F) Functional annotation analysis (DAVID) of the differentially expressed (up- and downregulated) genes. (G) Log 2 fold change of expression genes involved in kidney development. Asterisks represent FDR significant differences calculated by DESeq2. * P

    Article Snippet: Immunostaining were performed using the following primary antibodies: DNMT1 (ab188453; Abcam), SIX2 (11562–1-AP; Proteintech), p-53 (#2526; CST), fluorescein labeled Peanut agglutinin (PNA), Lotus tetragonolobus lectin (LTL), and Dolichos biflorus agglutinin (DBA) (FL-1071, FL-1321, FL-1031; Vector) after heat-induced antigen retrieval by Tris-EDTA buffer (pH 9.0 or 6.0).

    Techniques: Cell Differentiation, Flow Cytometry, Expressing, Quantitative RT-PCR, Mouse Assay, Functional Assay

    Methylation changes in Six2 Cre Dnmt1 f/f mice are associated with embryonic, ectopic lineage and transposable element expression. (A) The number of identified DMR and DEGs and their consistency and directionality in control and Six2 Cre Dnmt1 f/f mice. (B) Representative DMRs and their target gene expression changes. DMRs are marked by red boxes. Left panel shows a UCSC genome browser screenshot with DNA methylation patterns and y -axis represents methylation level from 0% to 100%. Right panel shows gene expression level and x -axis represents normalized sequencing reads. (C) Tissue enrichment analysis of the target genes (DAVID). (D) Heatmap of the differentially expressed TEs between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. Color scheme uses z-score distribution. (E) Representative DMRs and their target TE expression changes. DMRs are marked by red boxes. Left panel shows a UCSC genome browser screenshot with DNA methylation patterns and y -axis represents methylation level from 0% to 100%. Right panel shows TE expression level and x -axis represents normalized sequencing reads.

    Journal: Journal of the American Society of Nephrology : JASN

    Article Title: DNMT1 in Six2 Progenitor Cells Is Essential for Transposable Element Silencing and Kidney Development

    doi: 10.1681/ASN.2018070687

    Figure Lengend Snippet: Methylation changes in Six2 Cre Dnmt1 f/f mice are associated with embryonic, ectopic lineage and transposable element expression. (A) The number of identified DMR and DEGs and their consistency and directionality in control and Six2 Cre Dnmt1 f/f mice. (B) Representative DMRs and their target gene expression changes. DMRs are marked by red boxes. Left panel shows a UCSC genome browser screenshot with DNA methylation patterns and y -axis represents methylation level from 0% to 100%. Right panel shows gene expression level and x -axis represents normalized sequencing reads. (C) Tissue enrichment analysis of the target genes (DAVID). (D) Heatmap of the differentially expressed TEs between Dnmt1 f/f and Six2 Cre Dnmt1 f/f mice. Color scheme uses z-score distribution. (E) Representative DMRs and their target TE expression changes. DMRs are marked by red boxes. Left panel shows a UCSC genome browser screenshot with DNA methylation patterns and y -axis represents methylation level from 0% to 100%. Right panel shows TE expression level and x -axis represents normalized sequencing reads.

    Article Snippet: Immunostaining were performed using the following primary antibodies: DNMT1 (ab188453; Abcam), SIX2 (11562–1-AP; Proteintech), p-53 (#2526; CST), fluorescein labeled Peanut agglutinin (PNA), Lotus tetragonolobus lectin (LTL), and Dolichos biflorus agglutinin (DBA) (FL-1071, FL-1321, FL-1031; Vector) after heat-induced antigen retrieval by Tris-EDTA buffer (pH 9.0 or 6.0).

    Techniques: Methylation, Mouse Assay, Expressing, DNA Methylation Assay, Sequencing

    ILK controls lymphatic vascular growth and VEGFR3 tyrosine phosphorylation in adult mice LSM images of a whole‐mount stained adult Prox1‐Cre ERT2 ;Ilk +/+ mouse ear (referred to as “adult control”) and Prox1‐Cre ERT2 ;Ilk ∆/∆ mouse ear (referred to as “adult ILK K.O.”), with higher magnification images indicated by dashed lines. Scale bars: 500 and 100 μm, respectively. LSM images of a whole‐mount stained adult control and ILK K.O. ear, with higher magnification images indicated by dashed lines. Arrows point to proliferating LECs. Scale bars: 100 and 20 μm, respectively. Dermal lymph vessel density as determined by VEGFR3‐positive area normalised to the total analysed area of adult control or ILK K.O. mice ( n = 4 control and n = 5 ILK K.O. mice), * P = 0.025. LEC proliferation as determined by phospho‐Histone H3‐positive LECs normalised to analysed VEGFR3‐positive area in the skin of adult control or ILK K.O. mice ( n = 7 control and n = 5 ILK K.O. mice), * P = 0.004. VEGFR3 tyrosine phosphorylation as determined by ELISA of skin lysates of adult control or ILK K.O. mice ( n = 3 mice per genotype), P = 0.062. LSM images of a whole‐mount stained adult control and ILK K.O. cornea, with detailed images on their right (L′, M′). Arrows point to lymph vessels protruding into the cornea (encircled by a dotted line). Scale bars: 500 μm and 100 μm, respectively. Number of lymph vessels in control or ILK K.O. corneas ( n = 5 and n = 7 corneas), * P = 0.02. Data information: Data are presented as means ± SEM, shown as percentage of control mice, unpaired two‐tailed Student's t ‐test.

    Journal: The EMBO Journal

    Article Title: Identification of ILK as a critical regulator of VEGFR3 signalling and lymphatic vascular growth

    doi: 10.15252/embj.201899322

    Figure Lengend Snippet: ILK controls lymphatic vascular growth and VEGFR3 tyrosine phosphorylation in adult mice LSM images of a whole‐mount stained adult Prox1‐Cre ERT2 ;Ilk +/+ mouse ear (referred to as “adult control”) and Prox1‐Cre ERT2 ;Ilk ∆/∆ mouse ear (referred to as “adult ILK K.O.”), with higher magnification images indicated by dashed lines. Scale bars: 500 and 100 μm, respectively. LSM images of a whole‐mount stained adult control and ILK K.O. ear, with higher magnification images indicated by dashed lines. Arrows point to proliferating LECs. Scale bars: 100 and 20 μm, respectively. Dermal lymph vessel density as determined by VEGFR3‐positive area normalised to the total analysed area of adult control or ILK K.O. mice ( n = 4 control and n = 5 ILK K.O. mice), * P = 0.025. LEC proliferation as determined by phospho‐Histone H3‐positive LECs normalised to analysed VEGFR3‐positive area in the skin of adult control or ILK K.O. mice ( n = 7 control and n = 5 ILK K.O. mice), * P = 0.004. VEGFR3 tyrosine phosphorylation as determined by ELISA of skin lysates of adult control or ILK K.O. mice ( n = 3 mice per genotype), P = 0.062. LSM images of a whole‐mount stained adult control and ILK K.O. cornea, with detailed images on their right (L′, M′). Arrows point to lymph vessels protruding into the cornea (encircled by a dotted line). Scale bars: 500 μm and 100 μm, respectively. Number of lymph vessels in control or ILK K.O. corneas ( n = 5 and n = 7 corneas), * P = 0.02. Data information: Data are presented as means ± SEM, shown as percentage of control mice, unpaired two‐tailed Student's t ‐test.

    Article Snippet: The following antibodies were used for immunostaining: goat anti‐mouse Lyve‐1 (R & D Systems, AF2125), rabbit anti‐mouse Lyve1 (Abcam, ab14917), rat anti‐mouse CD31/PECAM‐1 (BD Bioscience, 553370), goat anti‐CD31 (R & D Systems, AF3628), rabbit anti‐Prox1 (Proteintech, 11067‐2‐AP) and rat anti‐CD68 (Invitrogen, 14‐0681‐82).

    Techniques: Mouse Assay, Staining, Enzyme-linked Immunosorbent Assay, Two Tailed Test

    ILK controls the number of Ki67/Prox1‐positive LECs in the jls/pTD LSM images of stained cross‐sections through the jls/pTD of an E13.5 Flk1‐Cre;Ilk ∆/+ embryo (referred to as “control”) and an E13.5 Flk1‐Cre;Ilk ∆/∆ embryo (referred to as “ILK K.O.”). Arrowheads point to Ki67‐positive LECs. Scale bars: 20 μm. LEC proliferation as determined by the number of Ki67/Prox1 double‐positive LECs per jls/pTD section in E13.5 control or ILK K.O. embryos ( n = 8 control and n = 7 ILK K.O. embryos), * P = 0.024. Data information: Data are presented as means ± SEM, shown as percentage of control embryos, unpaired two‐tailed Student's t ‐test.

    Journal: The EMBO Journal

    Article Title: Identification of ILK as a critical regulator of VEGFR3 signalling and lymphatic vascular growth

    doi: 10.15252/embj.201899322

    Figure Lengend Snippet: ILK controls the number of Ki67/Prox1‐positive LECs in the jls/pTD LSM images of stained cross‐sections through the jls/pTD of an E13.5 Flk1‐Cre;Ilk ∆/+ embryo (referred to as “control”) and an E13.5 Flk1‐Cre;Ilk ∆/∆ embryo (referred to as “ILK K.O.”). Arrowheads point to Ki67‐positive LECs. Scale bars: 20 μm. LEC proliferation as determined by the number of Ki67/Prox1 double‐positive LECs per jls/pTD section in E13.5 control or ILK K.O. embryos ( n = 8 control and n = 7 ILK K.O. embryos), * P = 0.024. Data information: Data are presented as means ± SEM, shown as percentage of control embryos, unpaired two‐tailed Student's t ‐test.

    Article Snippet: The following antibodies were used for immunostaining: goat anti‐mouse Lyve‐1 (R & D Systems, AF2125), rabbit anti‐mouse Lyve1 (Abcam, ab14917), rat anti‐mouse CD31/PECAM‐1 (BD Bioscience, 553370), goat anti‐CD31 (R & D Systems, AF3628), rabbit anti‐Prox1 (Proteintech, 11067‐2‐AP) and rat anti‐CD68 (Invitrogen, 14‐0681‐82).

    Techniques: Staining, Two Tailed Test

    LEC‐specific Ilk deletion confirms ILK‐controlled LEC proliferation in the jls/pTD LSM images of stained cross‐sections through the jls/pTD of an E13.5 Prox1‐Cre ERT2 ;Ilk +/+ embryo (referred to as “control”) and an E13.5 Prox1‐Cre ERT2 ;Ilk ∆/∆ embryo (referred to as “induced ILK K.O.”). Arrowheads point to phospho‐Histone H3‐positive LECs. Scale bars: 20 μm. LEC proliferation as determined by the number of phospho‐Histone H3‐/Prox1‐positive LECs per jls/pTD section in E13.5 control or induced ILK K.O. embryos ( n = 7 control and n = 8 induced ILK K.O. embryos), * P = 0.004. LEC proliferation normalised to total Prox1‐positive LECs in E13.5 control or induced ILK K.O. embryos ( n = 7 control and n = 8 induced ILK K.O. embryos), * P = 0.012. Data information: Data are presented as means ± SEM, shown as percentage of control embryos, unpaired two‐tailed Student's t ‐test.

    Journal: The EMBO Journal

    Article Title: Identification of ILK as a critical regulator of VEGFR3 signalling and lymphatic vascular growth

    doi: 10.15252/embj.201899322

    Figure Lengend Snippet: LEC‐specific Ilk deletion confirms ILK‐controlled LEC proliferation in the jls/pTD LSM images of stained cross‐sections through the jls/pTD of an E13.5 Prox1‐Cre ERT2 ;Ilk +/+ embryo (referred to as “control”) and an E13.5 Prox1‐Cre ERT2 ;Ilk ∆/∆ embryo (referred to as “induced ILK K.O.”). Arrowheads point to phospho‐Histone H3‐positive LECs. Scale bars: 20 μm. LEC proliferation as determined by the number of phospho‐Histone H3‐/Prox1‐positive LECs per jls/pTD section in E13.5 control or induced ILK K.O. embryos ( n = 7 control and n = 8 induced ILK K.O. embryos), * P = 0.004. LEC proliferation normalised to total Prox1‐positive LECs in E13.5 control or induced ILK K.O. embryos ( n = 7 control and n = 8 induced ILK K.O. embryos), * P = 0.012. Data information: Data are presented as means ± SEM, shown as percentage of control embryos, unpaired two‐tailed Student's t ‐test.

    Article Snippet: The following antibodies were used for immunostaining: goat anti‐mouse Lyve‐1 (R & D Systems, AF2125), rabbit anti‐mouse Lyve1 (Abcam, ab14917), rat anti‐mouse CD31/PECAM‐1 (BD Bioscience, 553370), goat anti‐CD31 (R & D Systems, AF3628), rabbit anti‐Prox1 (Proteintech, 11067‐2‐AP) and rat anti‐CD68 (Invitrogen, 14‐0681‐82).

    Techniques: Staining, Two Tailed Test

    LEC‐specific deletion of Ilk confirms ILK‐controlled VEGFR3 signalling LSM images of stained cross‐sections through the jls/pTD of an E13.5 Prox1‐Cre ERT2 ;Ilk +/+ embryo (referred to as “control”) and an E13.5 Prox1‐Cre ERT2 ;Ilk ∆/∆ embryo (referred to as “induced ILK K.O.”). Red dots indicate sites of tyrosine phosphorylation (p‐Tyr) in proximity to VEGFR3. Arrowheads point to PLA dots within the Lyve1‐stained area. Scale bars: 10 μm. Quantification of the PLA dots indicating VEGFR3 with phosphorylated tyrosine (p‐Tyr) per LEC in E13.5 control or induced ILK K.O. embryos ( n = 7 control and n = 8 induced ILK K.O. embryos), * P = 0.035. Data information: Data are presented as means ± SEM, shown as percentage of control embryos, unpaired two‐tailed Student's t ‐test.

    Journal: The EMBO Journal

    Article Title: Identification of ILK as a critical regulator of VEGFR3 signalling and lymphatic vascular growth

    doi: 10.15252/embj.201899322

    Figure Lengend Snippet: LEC‐specific deletion of Ilk confirms ILK‐controlled VEGFR3 signalling LSM images of stained cross‐sections through the jls/pTD of an E13.5 Prox1‐Cre ERT2 ;Ilk +/+ embryo (referred to as “control”) and an E13.5 Prox1‐Cre ERT2 ;Ilk ∆/∆ embryo (referred to as “induced ILK K.O.”). Red dots indicate sites of tyrosine phosphorylation (p‐Tyr) in proximity to VEGFR3. Arrowheads point to PLA dots within the Lyve1‐stained area. Scale bars: 10 μm. Quantification of the PLA dots indicating VEGFR3 with phosphorylated tyrosine (p‐Tyr) per LEC in E13.5 control or induced ILK K.O. embryos ( n = 7 control and n = 8 induced ILK K.O. embryos), * P = 0.035. Data information: Data are presented as means ± SEM, shown as percentage of control embryos, unpaired two‐tailed Student's t ‐test.

    Article Snippet: The following antibodies were used for immunostaining: goat anti‐mouse Lyve‐1 (R & D Systems, AF2125), rabbit anti‐mouse Lyve1 (Abcam, ab14917), rat anti‐mouse CD31/PECAM‐1 (BD Bioscience, 553370), goat anti‐CD31 (R & D Systems, AF3628), rabbit anti‐Prox1 (Proteintech, 11067‐2‐AP) and rat anti‐CD68 (Invitrogen, 14‐0681‐82).

    Techniques: Staining, Proximity Ligation Assay, Two Tailed Test

    ILK controls lymphatic vascular growth in the heart after myocardial infarction LSM images of cross‐sections through the heart of an adult Prox1‐Cre ERT2 ;Ilk +/+ mouse (referred to as “adult control”) and Prox1‐Cre ERT2 ;Ilk ∆/∆ mouse (referred to as “adult ILK K.O.”) showing the outer lateral region of the left ventricle (LV). Scale bars: 100 μm. Overall cardiac lymph vessel and blood vessel density in heart sections as determined by Lyve1‐positive and CD31‐positive area (normalised to total analysed myocardial area), respectively ( n = 4 control and n = 5 ILK K.O. mice). LSM images of cross‐sections through the heart of an adult control and ILK K.O. mouse 4 weeks after myocardial ischaemia and reperfusion (MI/R), showing the outer lateral region of the LV. Scale bars: 100 μm. Overall cardiac lymph vessel and blood vessel density in heart sections as determined by Lyve1‐positive and CD31‐positive area (normalised to total analysed myocardial area), respectively ( n = 5 control and n = 7 ILK K.O. mice), P = 0.051 (cardiac lymph vessel density in adult control or adult ILK K.O.), * P = 0.025 (cardiac blood vessel density in adult control or adult ILK K.O.). Data information: Data are presented as means ± SEM, shown as percentage of control mice, unpaired two‐tailed Student's t ‐test.

    Journal: The EMBO Journal

    Article Title: Identification of ILK as a critical regulator of VEGFR3 signalling and lymphatic vascular growth

    doi: 10.15252/embj.201899322

    Figure Lengend Snippet: ILK controls lymphatic vascular growth in the heart after myocardial infarction LSM images of cross‐sections through the heart of an adult Prox1‐Cre ERT2 ;Ilk +/+ mouse (referred to as “adult control”) and Prox1‐Cre ERT2 ;Ilk ∆/∆ mouse (referred to as “adult ILK K.O.”) showing the outer lateral region of the left ventricle (LV). Scale bars: 100 μm. Overall cardiac lymph vessel and blood vessel density in heart sections as determined by Lyve1‐positive and CD31‐positive area (normalised to total analysed myocardial area), respectively ( n = 4 control and n = 5 ILK K.O. mice). LSM images of cross‐sections through the heart of an adult control and ILK K.O. mouse 4 weeks after myocardial ischaemia and reperfusion (MI/R), showing the outer lateral region of the LV. Scale bars: 100 μm. Overall cardiac lymph vessel and blood vessel density in heart sections as determined by Lyve1‐positive and CD31‐positive area (normalised to total analysed myocardial area), respectively ( n = 5 control and n = 7 ILK K.O. mice), P = 0.051 (cardiac lymph vessel density in adult control or adult ILK K.O.), * P = 0.025 (cardiac blood vessel density in adult control or adult ILK K.O.). Data information: Data are presented as means ± SEM, shown as percentage of control mice, unpaired two‐tailed Student's t ‐test.

    Article Snippet: The following antibodies were used for immunostaining: goat anti‐mouse Lyve‐1 (R & D Systems, AF2125), rabbit anti‐mouse Lyve1 (Abcam, ab14917), rat anti‐mouse CD31/PECAM‐1 (BD Bioscience, 553370), goat anti‐CD31 (R & D Systems, AF3628), rabbit anti‐Prox1 (Proteintech, 11067‐2‐AP) and rat anti‐CD68 (Invitrogen, 14‐0681‐82).

    Techniques: Mouse Assay, Two Tailed Test