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Image Search Results
Journal: medRxiv
Article Title: Polymorphism in IFNAR contributes to glucocorticoid response and outcome in ARDS and COVID-19
doi: 10.1101/2022.03.10.22272123
Figure Lengend Snippet: (A ) STAT1 expression in the lung after 4-day culture in the presence of IFN beta with or without hydrocortisone (HC). ( B) pSTAT1 expression in the same specimens as in A. ( C) Example photomicrographs showing higher STAT2 expression in a TT patient than in a CT patient and the effect of HC on its nuclear translocation. Most STAT2 remains in the cytoplasm of the CT patients, whereas nuclear expression is prominent in the TT patient. Indicated insets are shown in the bottom row. Arrows. ( D ) Combined results of all patients noting that two CT samples are excluded in the data as the patients were already under glucocorticoid treatment at the time of sample acquisition. Ns, not significant; *P<0.05; **P<0.01; and ***P<0.001
Article Snippet: The first stage antibodies were anti-alpha chain of the IFN alpha/beta receptor (
Techniques: Expressing, Translocation Assay
Journal: Aging (Albany NY)
Article Title: Fibroblast growth factor 23 expression in human calcified vascular tissues
doi: 10.18632/aging.102297
Figure Lengend Snippet: von Kossa and immunohistochemichal staining for FGF23, FGFR1, FGFR3 and Klotho, in sections of calcified and not calcified arteries of vascular surgery patients and in sections of control donors (magnification 4x).
Article Snippet: Primary antibodies used were: rabbit polyclonal anti-FGF23, 1:250 dilution (Bi-Orbit);
Techniques: Staining
Journal: Aging (Albany NY)
Article Title: Fibroblast growth factor 23 expression in human calcified vascular tissues
doi: 10.18632/aging.102297
Figure Lengend Snippet: Differences in the log-transformed immunoreactivity levels of FGF23, Klotho, FGFR1 and FGFR3 attending to the presence of calcification. *P<0.01 vs. control group; #P<0.05 vs. non-calcified group.
Article Snippet: Primary antibodies used were: rabbit polyclonal anti-FGF23, 1:250 dilution (Bi-Orbit);
Techniques: Transformation Assay
Journal: Aging (Albany NY)
Article Title: Fibroblast growth factor 23 expression in human calcified vascular tissues
doi: 10.18632/aging.102297
Figure Lengend Snippet: Immunoreactivity quantification and gene expression study stratified by tertiles of soluble iFGF23 (pg/mL) and cFGF23 (RU/mL) levels.
Article Snippet: Primary antibodies used were: rabbit polyclonal anti-FGF23, 1:250 dilution (Bi-Orbit);
Techniques: Expressing
Journal: Investigative Ophthalmology & Visual Science
Article Title: Goblet Cell Differentiation Potential in Human Corneal Limbal Epithelial Progenitor Cells In Vitro
doi: 10.1167/iovs.61.12.27
Figure Lengend Snippet: FGFR, Fibroblast Growth Factor Receptor
Article Snippet: The following Abs were used: mouse anti-cytokeratin-3/2p monoclonal antibody (mAb; AE-5, 1:100; Santa Cruz Biotechnology, Inc, Dallas, TX, USA), mouse anti-human cytokeratin-4 mAb (6B10, 1:300; Abcam, Cambridge, UK), rabbit monoclonal [EP1599Y] anti-human cytokeratin 4 (1:200, Abcam), mouse anti-human cytokeratin-7 mAb (RCK105, 1:10000; Millipore, Billerica, MA, USA), mouse anti-human cytokeratin-13 mAb (1:20; American Research Products, Inc., Palos Verdes, CA, USA), mouse anti-human cytokeratin-12 mAb (N-16; 1:500; Santa Cruz Biotechnology), rabbit anti-cytokeratin 12/K12 mAb (1:200, EPR17882, Abcam), rabbit anti-human MUC5AC polyclonal Ab (H-160, 1:100, Santa Cruz Biotechnology),
Techniques:
Journal: Investigative Ophthalmology & Visual Science
Article Title: Goblet Cell Differentiation Potential in Human Corneal Limbal Epithelial Progenitor Cells In Vitro
doi: 10.1167/iovs.61.12.27
Figure Lengend Snippet: FGF receptor expression and effect of FGF receptor blockade in colonies derived from adherent single cells. ( A ) FGFR1 and FGFR2, but not FGFR3 and FGFR4, are detected in the adherent colonies by RT-PCR. ( B ) FGFR1 and FGFR2 expression is detected by Western blotting. ( C ) Effect of FGF receptor blockade was tested in colonies derived from adherent single cells. PAS-positive colony number in the anti-FGFR1 monoclonal antibody group significantly decreases as compared with that in the control Ig group. Treatment with an anti-FGFR2 blocking mAb does not affect the number of colony. ( D ) Colony with amorphous material and epithelium is observed with control IgG. ( E ) Anti-FGFR1 mAb suppresses the proliferation of both goblet-like cell and epithelium. Similar results were obtained with repeated three experiments. M, size markers; S, sample; P, positive control; N, negative control, N.S., not significant.
Article Snippet: The following Abs were used: mouse anti-cytokeratin-3/2p monoclonal antibody (mAb; AE-5, 1:100; Santa Cruz Biotechnology, Inc, Dallas, TX, USA), mouse anti-human cytokeratin-4 mAb (6B10, 1:300; Abcam, Cambridge, UK), rabbit monoclonal [EP1599Y] anti-human cytokeratin 4 (1:200, Abcam), mouse anti-human cytokeratin-7 mAb (RCK105, 1:10000; Millipore, Billerica, MA, USA), mouse anti-human cytokeratin-13 mAb (1:20; American Research Products, Inc., Palos Verdes, CA, USA), mouse anti-human cytokeratin-12 mAb (N-16; 1:500; Santa Cruz Biotechnology), rabbit anti-cytokeratin 12/K12 mAb (1:200, EPR17882, Abcam), rabbit anti-human MUC5AC polyclonal Ab (H-160, 1:100, Santa Cruz Biotechnology),
Techniques: Expressing, Derivative Assay, Reverse Transcription Polymerase Chain Reaction, Western Blot, Control, Blocking Assay, Positive Control, Negative Control
Journal: ESMO Open
Article Title: FGFR1-amplified colorectal cancer: a distinct prognostic subtype identified through integrated genomic and immunohistochemical profiling
doi: 10.1016/j.esmoop.2025.105561
Figure Lengend Snippet: Prognostic impact of FGFR1 amplification in CRC patients. KM curves of DFS (A) for stage I–III CRC patients and PFS (B) for stage IV CRC patients with FGFR1 , FGFR2 , and FGFR3 alterations. KM curve of DFS (C) for stage I–III CRC patients and PFS (D) for stage IV CRC patients with or without FGFR1 amplifications. (E) Swimmer plot of survival outcomes and therapy-related events in patients with FGFR1 amplifications compared with those with non-amplified FGFR alterations (including FGFR1 mutations and FGFR2 and FGFR3 alterations). CRC, colorectal cancer; DFS, disease-free survival; FGFR, fibroblast growth factor receptor; HR, hazard ratio; KM, Kaplan–Meier; PFS, progression-free survival
Article Snippet: Formalin-fixed and paraffin-embedded tumor samples were sectioned into 3-mm slices and incubated with an
Techniques: Amplification
Journal: ESMO Open
Article Title: FGFR1-amplified colorectal cancer: a distinct prognostic subtype identified through integrated genomic and immunohistochemical profiling
doi: 10.1016/j.esmoop.2025.105561
Figure Lengend Snippet: IHC detection of FGFR1 in tumor tissues and consistency with FGFR1 gene amplification. (A) Concordance of the FGFR1 mRNA level (Z score) with the FGFR1 copy number status (diploid or amplified) in the TCGA-CRC cohort. (B) IHC assessment of FGFR1 expression in 8 FGFR 1 -amplified and 13 non-amplified tumor samples, which were evaluated using three scoring methods: the H score, IRS, and cytonuclear score. (C) Concordance of the FGFR1 IHC H score with FGFR1 amplification. (D) Representative IHC images (×4 and ×40) illustrating FGFR1 expression levels, as classified via the IRS method. CRC, colorectal cancer; FGFR1, fibroblast growth factor receptor 1; IHC, immunohistochemistry; IRS, immunoreactive score; TCGA, The Cancer Genome Atlas.
Article Snippet: Formalin-fixed and paraffin-embedded tumor samples were sectioned into 3-mm slices and incubated with an
Techniques: Amplification, Expressing, Immunohistochemistry
Journal: Molecular Therapy. Nucleic Acids
Article Title: Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis
doi: 10.1016/j.omtn.2021.10.003
Figure Lengend Snippet: miR-22 targets SIRT1 and FGFR1 in ECs (A) mRNA levels (in % of NCm) of putative and validated human target genes of miR-22 in NCm- or miR-22m-transfected HDMECs, as assessed by real-time PCR (n = 3). (B) Western blots of SIRT1, FGFR1, and β-actin expression in HDMECs transfected with NCm or miR-22m. (C) Expression level (in % of NCm) of SIRT1/β-actin and FGFR1/β-actin, as assessed by western blotting (n = 3). (D) Luciferase activity (in % of NCm) in 293T cells cotransfected with NCm or miR-22m and a reporter plasmid carrying mutant or wild-type FGFR1 -3′ UTR, as assessed by the luciferase assay (n = 4). (E) Western blots of p-AKT, AKT, p-mTOR, mTOR, and β-actin expression in HDMECs transfected with NCm or miR-22m. (F and G) Expression levels (in % of NCm) of p-AKT/AKT (F) and p-mTOR/mTOR (G), as assessed by western blotting (n = 3). Data are means ± SEM. ∗p < 0.05 versus NCm.
Article Snippet: The membranes were blocked and incubated overnight at 4°C with a
Techniques: Transfection, Real-time Polymerase Chain Reaction, Western Blot, Expressing, Luciferase, Activity Assay, Plasmid Preparation, Mutagenesis
Journal: Molecular Therapy. Nucleic Acids
Article Title: Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis
doi: 10.1016/j.omtn.2021.10.003
Figure Lengend Snippet: miR-22 inhibits angiogenesis through targeting SIRT1 and FGFR1 (A and B) Viability (in % of 0 μM or 0 nM) of HDMECs that were exposed for 72 h to serial dilutions of EX-527 (A) and PD173074 (B), as assessed by the WST-1 assay (n = 3). (C) Viability (in % of NCi) of HDMECs that were transfected with NCi or miR-22i and then treated with 10 μM of EX-527 (EX) or 50 nM of PD173074 (PD) for 72 h, as assessed by the WST-1 assay (n = 4). (D) Wound area (in % of 0 h) created by scratching the monolayer of HDMECs that were transfected with NCi or miR-22i and then treated with 10 μM of EX-527 or 50 nM of PD173074 for 12 h, as assessed by the scratch wound healing assay (n = 6 to 7). (E) Tube formation (in % of NCi) of HDMECs that were transfected with NCi or miR-22i and then treated with 10 μM of EX-527 or 50 nM of PD173074 for 18 h, as assessed by the tube formation assay (n = 5). (F) Viability (in % of NCi) of HDMECs that were transfected with NCi or miR-22i and then treated with 5 μM of MK-2206 (MK) for 72 h, as assessed by the WST-1 assay (n = 4). (G) Wound area (in % of 0 h) created by scratching the monolayer of HDMECs that were transfected with NCi or miR-22i and then treated with 5 μM of MK-2206 for 12 h, as assessed by the scratch wound healing assay (n = 6). (H) Tube formation (in % of NCi) of HDMECs that were transfected with NCi or miR-22i and then treated with 5 μM of MK-2206 for 18 h, as assessed by the tube formation assay (n = 4). (I and J) mRNA level of SIRT1 (I) or FGFR1 (J) (in % of Con) in HDMECs that were exposed for 72 h to vehicle (Con), 2 ng/mL of IL-1β, or 1 μM of Bay 11-7082 (Bay), as assessed by real-time PCR (n = 3). (K and L) mRNA level of SIRT1 (K) or FGFR1 (L) (in % of HDMEC) in HDMECs that were cultured alone (HDMEC) or cocultured with NCI-H460 cells [HDMEC (H460)] without contact in a transwell plate in the absence or presence of 1 μM of Bay 11-7082 (Bay) for 72 h, as assessed by real-time PCR (n = 3). Data are means ± SEM. ∗p < 0.05 versus 0 μM, 0 nM, NCi, Con, or HDMEC; # p < 0.05 versus miR-22i (C–H) or HDMEC (H460) (K and L).
Article Snippet: The membranes were blocked and incubated overnight at 4°C with a
Techniques: WST-1 Assay, Transfection, Wound Healing Assay, Tube Formation Assay, Real-time Polymerase Chain Reaction, Cell Culture
Journal: Molecular Therapy. Nucleic Acids
Article Title: Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis
doi: 10.1016/j.omtn.2021.10.003
Figure Lengend Snippet: NSCLC cells stimulate angiogenesis by downregulating endothelial miR-22, which targets SIRT1 and FGFR1 The scheme summarizes the underlying mechanisms, as outlined in detail in the .
Article Snippet: The membranes were blocked and incubated overnight at 4°C with a
Techniques:
Journal: bioRxiv
Article Title: Subcellular localization of glypican-5 associates with dynamic cell motility and cell communication of the human mesenchymal stem cell line U3DT
doi: 10.1101/863720
Figure Lengend Snippet: (A) U3DT cells at different stages of mitosis and cytokinesis were fixed but not permeabilized, stained with anti-GPC5 (red) and anti-FGFR1 (green) antibodies, and counterstained with DAPI stain (blue). Yellow represents the degree of colocalization. Scale bar, 5 μm. (B) Cells expressing the same marker as in (A) but with permeabilized cells. Scale bar, 5 μm.
Article Snippet: Antibodies and fluorescence-conjugated reagent used in this study are as follows; Anti-GPC5 antibody (MAB2607, R&D Systems, Inc.), Alexa Fluor 594-conjucated anti-GPC5 antibody (R&D Systems, Inc.), Alexa Fluor 647-conjucated anti-GPC5 antibody (R&D Systems, Inc.),
Techniques: Staining, Expressing, Marker
Journal: bioRxiv
Article Title: Subcellular localization of glypican-5 associates with dynamic cell motility and cell communication of the human mesenchymal stem cell line U3DT
doi: 10.1101/863720
Figure Lengend Snippet: (A–D) Images of staining with Alexa Fluor 488-conjugated WGA and DAPI at interphase (A), metaphase (B), and anaphase and telophase (C–D). (D) Maximum projection of 15 Z-staged-images stained with Alexa Fluor 488-WGA and DAPI. (E) U3DT cell at telophase, stained with anti-GPC5 antibody (red) and Alexa Fluor 488-WGA (green). (F) Blebs of U3DT cell at telophase stained with anti-FGFR1 (brown), Alexa Fluor 488-WGA (green), and DAPI (blue). (G) Blebs of U3DT cells at telophase stained with anti-Rab11A antibodies (magenta), Alexa Fluor 488-WGA (green), and DAPI (blue). Scale bar, 5 μm.
Article Snippet: Antibodies and fluorescence-conjugated reagent used in this study are as follows; Anti-GPC5 antibody (MAB2607, R&D Systems, Inc.), Alexa Fluor 594-conjucated anti-GPC5 antibody (R&D Systems, Inc.), Alexa Fluor 647-conjucated anti-GPC5 antibody (R&D Systems, Inc.),
Techniques: Staining
Journal: bioRxiv
Article Title: Subcellular localization of glypican-5 associates with dynamic cell motility and cell communication of the human mesenchymal stem cell line U3DT
doi: 10.1101/863720
Figure Lengend Snippet: (A) Electron microscopic image of negative-stained EVs. The inset shows a magnification of the boxed EV. (B) Size distribution of vesicles in EV preparations measured by image software (n = 110). (C) (F) (I) (L) GPC5-immunostained EVs (red) stained for Rab11 (green) (C), FGFR1 (green) (F), CD63 (green) (I), and ARF6 (green) (L). (D) (G) (J) (M) Line scan determination of the red bars in (C), (F), (I), and (L): GPC5 (red), others (green). (E) (H) (K) (N) Quantification of scan determinations in (D), (G), (J), and (M). n = 1,516, (E), 630 (H), 704 (K), and 406 (N). Scale bars: (A), 500 nm; (C), (F), (I), (L), 2 μm.
Article Snippet: Antibodies and fluorescence-conjugated reagent used in this study are as follows; Anti-GPC5 antibody (MAB2607, R&D Systems, Inc.), Alexa Fluor 594-conjucated anti-GPC5 antibody (R&D Systems, Inc.), Alexa Fluor 647-conjucated anti-GPC5 antibody (R&D Systems, Inc.),
Techniques: Staining, Software
Journal: bioRxiv
Article Title: Subcellular localization of glypican-5 associates with dynamic cell motility and cell communication of the human mesenchymal stem cell line U3DT
doi: 10.1101/863720
Figure Lengend Snippet: (A–B) Images of control cells. (C–D) Images of EV-treated cells. (B) (D) Merged images of UE6E7T-3 cells (B) and EV-treated cells (D) stained for GPC5 (red) and FGFR1 (green). (E) Histogram of GPC5 (pixel sum per cell) in control UE6E7T-3 cells (blue) or of cells cultured with EVs for 1 day (red). n = 29 (blue) and 46 (red). (F–G) FACS pattern of GPC5 in UE6E7T-3 cells (F) and in cells cultured with EVs for 1 day (G). Scale bar, 5 μm.
Article Snippet: Antibodies and fluorescence-conjugated reagent used in this study are as follows; Anti-GPC5 antibody (MAB2607, R&D Systems, Inc.), Alexa Fluor 594-conjucated anti-GPC5 antibody (R&D Systems, Inc.), Alexa Fluor 647-conjucated anti-GPC5 antibody (R&D Systems, Inc.),
Techniques: Staining, Cell Culture
Journal: Oncogene
Article Title: Genome-wide CRISPR screen identifies LGALS2 as an oxidative stress-responsive gene with an inhibitory function on colon tumor growth
doi: 10.1038/s41388-020-01523-5
Figure Lengend Snippet: A Western blotting showing the expression of p-STAT3 and STAT3 in healthy colon or colon tumors. B Densitometry quantification of p-STAT3/total STAT3 for colons or colorectal tumors. *** p < 0.001 (one-way ANOVA). C Representative images of p-STAT3 immunostaining of colons or colon tumors. Scale bar: 50 μm. D Quantification of p-STAT3 + cells in colon tumors of WT and Gal2-KO mice. *** p < 0.001 ( t -test).
Article Snippet: Primary antibodies including the goat polyclonal anti-Gal2 (STJ24400, 1:500,
Techniques: Western Blot, Expressing, Immunostaining
Journal: Oncogene
Article Title: Genome-wide CRISPR screen identifies LGALS2 as an oxidative stress-responsive gene with an inhibitory function on colon tumor growth
doi: 10.1038/s41388-020-01523-5
Figure Lengend Snippet: A Western blotting showing the expression of Gal2 in stable Gal2-overexpressing HCT116 cells. The red arrow indicates the un-cleaved GFP-2A-Gal2 fusion protein. B The CCK8 proliferation assay of HCT116 with or without Gal2 overexpression. C The survival assay of HCT116 with or without Gal2 overexpression in the presence of 0.6 mM H 2 O 2 . ** p < 0.01, *** p < 0.001 ( t -test). D Western blotting showing the expression of p-STAT3 and STAT3 in HCT116 cells with or without Gal2 overexpression. E Densitometry quantification of p-STAT3/total STAT3 in HCT116 cells with or without Gal2 overexpression. ** p < 0.01 (one-way ANOVA).
Article Snippet: Primary antibodies including the goat polyclonal anti-Gal2 (STJ24400, 1:500,
Techniques: Western Blot, Expressing, Proliferation Assay, Over Expression, Clonogenic Cell Survival Assay