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fgfr2  (Carna Inc)


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    Structured Review

    Carna Inc fgfr2
    Fgfr2, supplied by Carna Inc, used in various techniques. Bioz Stars score: 95/100, based on 559 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fgfr2/FGFR2/custom%4008-134%4042134161
    Average 95 stars, based on 559 article reviews
    fgfr2 - by Bioz Stars, 2026-11
    95/100 stars

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    Related Articles

    Activity Assay:

    Article Title: 2 H -pyrazolo[3,4- d ]pyrimidin-4-amine derivatives as novel selective fibroblast growth factor receptor 2 (FGFR2) inhibitors.
    Article Snippet: .. FGFR kinase activity inhibition assay PLW559 was preincubated with FGFR1, FGFR2, FGFR3 or FGFR4 kinase (carna Biosciences) and substrate peptide (Peptide30, Gl) in 50 mmol/l hePes, ph 7.5, 10 mmol/l Mgcl2, 1 mmol/l eGta, 0.01% Brij-35, 2 mmol/l Dtt, and 0.05% Bsa for 30 min at room temperature. compounds were transferred 200 nl of each well from the 384-well echo plate to a 384-well assay plate in duplicates by echo. atP was added to a total concentration of 100 μmol/l and incubated for a period of time, and reactions were stopped using 100 mmol/l hePes, ph 7.5, 50 mmol/l eDta, 0.015% Brij-35 and 0.2% coating reagent #3 (Perkinelmer). the substrate conversion ratio was calculated for each PlW559 concentration and was then used to calculate ic50 values. ..

    Inhibition:

    Article Title: 2 H -pyrazolo[3,4- d ]pyrimidin-4-amine derivatives as novel selective fibroblast growth factor receptor 2 (FGFR2) inhibitors.
    Article Snippet: .. FGFR kinase activity inhibition assay PLW559 was preincubated with FGFR1, FGFR2, FGFR3 or FGFR4 kinase (carna Biosciences) and substrate peptide (Peptide30, Gl) in 50 mmol/l hePes, ph 7.5, 10 mmol/l Mgcl2, 1 mmol/l eGta, 0.01% Brij-35, 2 mmol/l Dtt, and 0.05% Bsa for 30 min at room temperature. compounds were transferred 200 nl of each well from the 384-well echo plate to a 384-well assay plate in duplicates by echo. atP was added to a total concentration of 100 μmol/l and incubated for a period of time, and reactions were stopped using 100 mmol/l hePes, ph 7.5, 50 mmol/l eDta, 0.015% Brij-35 and 0.2% coating reagent #3 (Perkinelmer). the substrate conversion ratio was calculated for each PlW559 concentration and was then used to calculate ic50 values. ..

    Concentration Assay:

    Article Title: 2 H -pyrazolo[3,4- d ]pyrimidin-4-amine derivatives as novel selective fibroblast growth factor receptor 2 (FGFR2) inhibitors.
    Article Snippet: .. FGFR kinase activity inhibition assay PLW559 was preincubated with FGFR1, FGFR2, FGFR3 or FGFR4 kinase (carna Biosciences) and substrate peptide (Peptide30, Gl) in 50 mmol/l hePes, ph 7.5, 10 mmol/l Mgcl2, 1 mmol/l eGta, 0.01% Brij-35, 2 mmol/l Dtt, and 0.05% Bsa for 30 min at room temperature. compounds were transferred 200 nl of each well from the 384-well echo plate to a 384-well assay plate in duplicates by echo. atP was added to a total concentration of 100 μmol/l and incubated for a period of time, and reactions were stopped using 100 mmol/l hePes, ph 7.5, 50 mmol/l eDta, 0.015% Brij-35 and 0.2% coating reagent #3 (Perkinelmer). the substrate conversion ratio was calculated for each PlW559 concentration and was then used to calculate ic50 values. ..

    Incubation:

    Article Title: 2 H -pyrazolo[3,4- d ]pyrimidin-4-amine derivatives as novel selective fibroblast growth factor receptor 2 (FGFR2) inhibitors.
    Article Snippet: .. FGFR kinase activity inhibition assay PLW559 was preincubated with FGFR1, FGFR2, FGFR3 or FGFR4 kinase (carna Biosciences) and substrate peptide (Peptide30, Gl) in 50 mmol/l hePes, ph 7.5, 10 mmol/l Mgcl2, 1 mmol/l eGta, 0.01% Brij-35, 2 mmol/l Dtt, and 0.05% Bsa for 30 min at room temperature. compounds were transferred 200 nl of each well from the 384-well echo plate to a 384-well assay plate in duplicates by echo. atP was added to a total concentration of 100 μmol/l and incubated for a period of time, and reactions were stopped using 100 mmol/l hePes, ph 7.5, 50 mmol/l eDta, 0.015% Brij-35 and 0.2% coating reagent #3 (Perkinelmer). the substrate conversion ratio was calculated for each PlW559 concentration and was then used to calculate ic50 values. ..

    Article Title: rlay-10k_20201231.htm
    Article Snippet: The selectivity of RLY-4008 for FGFR2 over FGFR1 was determined by comparing the potency (IC50) of RLY-4008 and other clinical non-selective FGFR inhibitors in biochemical assays using Caliper technology (PerkinElmer). .. Human FGFR1 and FGFR2 (Carna Biosciences) were incubated with a peptide substrate (PerkinElmer) in the presence of varying concentrations of the indicated inhibitor for 30 minutes. ..



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    Image Search Results


    FGF–FGFR‐mediated endothelial–tumour crosstalk. (A) Uniform manifold approximation and projection (UMAP) plots showing annotation of endothelial cell subpopulations. (B) Bubble plots displaying marker genes used for endothelial subpopulation annotation. (C) Pseudotime trajectory analysis of endothelial cells, showing differentiation progression. (D) Box plots comparing differentiation states among endothelial subpopulations. (E) CytoTRACE analysis depicting differentiation status across endothelial subpopulations. (F) Heatmap of branch‐dependent highly expressed genes along the endothelial pseudotime trajectory. (G) Circos‐style plot illustrating interaction strength between endothelial subpopulations and other major annotated cell types; arc thickness represents signal intensity. (H) Heatmap showing activation levels of the fibroblast growth factor (FGF)signalling pathway across endothelial subpopulations. (I) Cell–cell interaction heatmap displaying intercellular signalling activity. (J) NicheNet analysis showing ligand–receptor distribution between tumour cells and other cell types. (K) Expression distribution of FGFR1, FGFR2 and FGFR3 across different cell subclusters.

    Journal: Clinical and Translational Medicine

    Article Title: Neuro‐associated SEMA3C + tumour cells promote gastric cancer peritoneal metastasis via EBF2–FGF7–FGFR2‐mediated tumour–endothelial crosstalk

    doi: 10.1002/ctm2.70861

    Figure Lengend Snippet: FGF–FGFR‐mediated endothelial–tumour crosstalk. (A) Uniform manifold approximation and projection (UMAP) plots showing annotation of endothelial cell subpopulations. (B) Bubble plots displaying marker genes used for endothelial subpopulation annotation. (C) Pseudotime trajectory analysis of endothelial cells, showing differentiation progression. (D) Box plots comparing differentiation states among endothelial subpopulations. (E) CytoTRACE analysis depicting differentiation status across endothelial subpopulations. (F) Heatmap of branch‐dependent highly expressed genes along the endothelial pseudotime trajectory. (G) Circos‐style plot illustrating interaction strength between endothelial subpopulations and other major annotated cell types; arc thickness represents signal intensity. (H) Heatmap showing activation levels of the fibroblast growth factor (FGF)signalling pathway across endothelial subpopulations. (I) Cell–cell interaction heatmap displaying intercellular signalling activity. (J) NicheNet analysis showing ligand–receptor distribution between tumour cells and other cell types. (K) Expression distribution of FGFR1, FGFR2 and FGFR3 across different cell subclusters.

    Article Snippet: The antibodies used and their catalogue numbers are as follows: SEMA3C (Novus Biologicals, Cat# MAB1728), CD31 (Servicebio, Cat# GB11063‐1), VWF (Servicebio, Cat# GB11020), FGFR2 (Proteintech, Cat# 13042‐1‐AP), PDGFRβ (Epizyme, Cat# P012976), VEGFR2 (Epizyme, Cat# P013400), CK7 (Biodragon, Cat# BD‐PM3054), Ki67 (Servicebio, Cat# GB111499 ) and EBF2 (Affinity, Cat# DF13398).

    Techniques: Marker, Analysis, Activation Assay, Activity Assay, Expressing

    EBF2‐regulated tumour cell subpopulation mediates semaphorin 3C (SEMA3C) effects. (A) Bright‐field and haematoxylin and eosin (H&E) images showing interactions between tumour organoids and tumour‐associated endothelial cells (TECs) across different experimental groups (bright‐field scale bar: 100 µm; H&E scale bar: 20 µm). (B) Immunofluorescence images depicting the expression of relevant markers and the extent of organoid–endothelial cell interactions after co‐culture in different groups (scale bar: 30 µm). (C) Immunofluorescence images showing organoid–TEC interactions and marker expression across experimental conditions (scale bar: 30 µm). (D) pySCENIC analysis illustrating transcription factor activity within the SEMA3C + tumour cell subpopulation. (E) Tripartite plot displaying predicted target genes regulated by EBF2 in the SEMA3C + subpopulation. (F) Immunofluorescence images showing co‐staining of tumour cell subpopulation marker genes and predicted transcription factors under different experimental conditions (scale bar: 30 µm).

    Journal: Clinical and Translational Medicine

    Article Title: Neuro‐associated SEMA3C + tumour cells promote gastric cancer peritoneal metastasis via EBF2–FGF7–FGFR2‐mediated tumour–endothelial crosstalk

    doi: 10.1002/ctm2.70861

    Figure Lengend Snippet: EBF2‐regulated tumour cell subpopulation mediates semaphorin 3C (SEMA3C) effects. (A) Bright‐field and haematoxylin and eosin (H&E) images showing interactions between tumour organoids and tumour‐associated endothelial cells (TECs) across different experimental groups (bright‐field scale bar: 100 µm; H&E scale bar: 20 µm). (B) Immunofluorescence images depicting the expression of relevant markers and the extent of organoid–endothelial cell interactions after co‐culture in different groups (scale bar: 30 µm). (C) Immunofluorescence images showing organoid–TEC interactions and marker expression across experimental conditions (scale bar: 30 µm). (D) pySCENIC analysis illustrating transcription factor activity within the SEMA3C + tumour cell subpopulation. (E) Tripartite plot displaying predicted target genes regulated by EBF2 in the SEMA3C + subpopulation. (F) Immunofluorescence images showing co‐staining of tumour cell subpopulation marker genes and predicted transcription factors under different experimental conditions (scale bar: 30 µm).

    Article Snippet: The antibodies used and their catalogue numbers are as follows: SEMA3C (Novus Biologicals, Cat# MAB1728), CD31 (Servicebio, Cat# GB11063‐1), VWF (Servicebio, Cat# GB11020), FGFR2 (Proteintech, Cat# 13042‐1‐AP), PDGFRβ (Epizyme, Cat# P012976), VEGFR2 (Epizyme, Cat# P013400), CK7 (Biodragon, Cat# BD‐PM3054), Ki67 (Servicebio, Cat# GB111499 ) and EBF2 (Affinity, Cat# DF13398).

    Techniques: Organoids, Immunofluorescence, Expressing, Co-culture Assay, Marker, Analysis, Activity Assay, Staining

    Semaphorin 3C (SEMA3C) drives tumour expansion via FGFR2‐mediated endothelial interaction. (A) Schematic diagram of the patient‐derived organoids‐based xenograft (PDOX) model construction and drug administration protocol. (B) Representative gross images of tumours from PDOX models in different experimental groups ( n = 5 mice per group). (C) Bar graph showing tumour weights across different groups. (D) Bar graph showing tumour volumes across different groups. (E) Immunofluorescence images showing the expression of relevant markers in tumour samples from different groups (scale bar: 50 µm). (F) Quantification of Ki67‐positive cells in tumour samples across experimental groups. (G) Quantification of CK7‐positive cells in tumour samples across experimental groups. (H) Quantification of VEGFR2 fluorescence intensity in tumour samples across groups. (I) Quantification of FGFR2‐positive cells in tumour samples across groups.

    Journal: Clinical and Translational Medicine

    Article Title: Neuro‐associated SEMA3C + tumour cells promote gastric cancer peritoneal metastasis via EBF2–FGF7–FGFR2‐mediated tumour–endothelial crosstalk

    doi: 10.1002/ctm2.70861

    Figure Lengend Snippet: Semaphorin 3C (SEMA3C) drives tumour expansion via FGFR2‐mediated endothelial interaction. (A) Schematic diagram of the patient‐derived organoids‐based xenograft (PDOX) model construction and drug administration protocol. (B) Representative gross images of tumours from PDOX models in different experimental groups ( n = 5 mice per group). (C) Bar graph showing tumour weights across different groups. (D) Bar graph showing tumour volumes across different groups. (E) Immunofluorescence images showing the expression of relevant markers in tumour samples from different groups (scale bar: 50 µm). (F) Quantification of Ki67‐positive cells in tumour samples across experimental groups. (G) Quantification of CK7‐positive cells in tumour samples across experimental groups. (H) Quantification of VEGFR2 fluorescence intensity in tumour samples across groups. (I) Quantification of FGFR2‐positive cells in tumour samples across groups.

    Article Snippet: The antibodies used and their catalogue numbers are as follows: SEMA3C (Novus Biologicals, Cat# MAB1728), CD31 (Servicebio, Cat# GB11063‐1), VWF (Servicebio, Cat# GB11020), FGFR2 (Proteintech, Cat# 13042‐1‐AP), PDGFRβ (Epizyme, Cat# P012976), VEGFR2 (Epizyme, Cat# P013400), CK7 (Biodragon, Cat# BD‐PM3054), Ki67 (Servicebio, Cat# GB111499 ) and EBF2 (Affinity, Cat# DF13398).

    Techniques: Patient-Derived Organoids, Xenograft Assay, Immunofluorescence, Expressing, Fluorescence, Derivative Assay

    Therapeutic targeting of the EBF2–FGF7–FGFR2 signalling axis. (A) Representative gross images showing tumour sizes in patient‐derived xenograft (PDX) models across different experimental groups ( n = 5 mice per group). (B) Bar graphs depicting tumour weights and volumes in different groups. (C) Immunofluorescence images showing the expression of relevant markers in tumour samples from different groups (scale bar: 50 µm).

    Journal: Clinical and Translational Medicine

    Article Title: Neuro‐associated SEMA3C + tumour cells promote gastric cancer peritoneal metastasis via EBF2–FGF7–FGFR2‐mediated tumour–endothelial crosstalk

    doi: 10.1002/ctm2.70861

    Figure Lengend Snippet: Therapeutic targeting of the EBF2–FGF7–FGFR2 signalling axis. (A) Representative gross images showing tumour sizes in patient‐derived xenograft (PDX) models across different experimental groups ( n = 5 mice per group). (B) Bar graphs depicting tumour weights and volumes in different groups. (C) Immunofluorescence images showing the expression of relevant markers in tumour samples from different groups (scale bar: 50 µm).

    Article Snippet: The antibodies used and their catalogue numbers are as follows: SEMA3C (Novus Biologicals, Cat# MAB1728), CD31 (Servicebio, Cat# GB11063‐1), VWF (Servicebio, Cat# GB11020), FGFR2 (Proteintech, Cat# 13042‐1‐AP), PDGFRβ (Epizyme, Cat# P012976), VEGFR2 (Epizyme, Cat# P013400), CK7 (Biodragon, Cat# BD‐PM3054), Ki67 (Servicebio, Cat# GB111499 ) and EBF2 (Affinity, Cat# DF13398).

    Techniques: Derivative Assay, Xenograft Assay, Immunofluorescence, Expressing

    Schematic illustration summarising the key findings from single‐nucleus sequencing of gastric cancer peritoneal metastases. A tumour subpopulation with high semaphorin 3C (SEMA3C) expression was identified, which exhibits extensive interactions with tumour‐associated endothelial cells (TECs). TECs display high VEGFR2 expression, and transcriptional regulation by EBF2 in the tumour subpopulation leads to upregulation of FGF7. Tumour cells further interact with endothelial cells via the FGF7–FGFR2 signalling axis, promoting vascular remodelling, tumour proliferation and metastatic potential.

    Journal: Clinical and Translational Medicine

    Article Title: Neuro‐associated SEMA3C + tumour cells promote gastric cancer peritoneal metastasis via EBF2–FGF7–FGFR2‐mediated tumour–endothelial crosstalk

    doi: 10.1002/ctm2.70861

    Figure Lengend Snippet: Schematic illustration summarising the key findings from single‐nucleus sequencing of gastric cancer peritoneal metastases. A tumour subpopulation with high semaphorin 3C (SEMA3C) expression was identified, which exhibits extensive interactions with tumour‐associated endothelial cells (TECs). TECs display high VEGFR2 expression, and transcriptional regulation by EBF2 in the tumour subpopulation leads to upregulation of FGF7. Tumour cells further interact with endothelial cells via the FGF7–FGFR2 signalling axis, promoting vascular remodelling, tumour proliferation and metastatic potential.

    Article Snippet: The antibodies used and their catalogue numbers are as follows: SEMA3C (Novus Biologicals, Cat# MAB1728), CD31 (Servicebio, Cat# GB11063‐1), VWF (Servicebio, Cat# GB11020), FGFR2 (Proteintech, Cat# 13042‐1‐AP), PDGFRβ (Epizyme, Cat# P012976), VEGFR2 (Epizyme, Cat# P013400), CK7 (Biodragon, Cat# BD‐PM3054), Ki67 (Servicebio, Cat# GB111499 ) and EBF2 (Affinity, Cat# DF13398).

    Techniques: Sequencing, Expressing

    The effect of FGF7 on the ADAM17-EGFR-ERK1/2 signaling pathway in 16HBE cells. (A, B) Representative Western blots and densitometry for FGF7 and p-FGFR2/FGFR2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (C, D) Representative Western blots and densitometry for FGF7, ADAM17, p-p38/p38, and p-AKT/AKT under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (E, F) Representative Western blots and densitometry for ADAM17, p-EGFR/EGFR, and p-ERK1/2/ERK1/2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). Compared to Control, * P < 0.05; Compared to CSE, # P < 0.05; Compared to CSE+FGF7, & P < 0.05.

    Journal: Frontiers in Immunology

    Article Title: FGF7 mitigates airway inflammation and epithelial injury in cigarette smoke-induced COPD model

    doi: 10.3389/fimmu.2026.1815550

    Figure Lengend Snippet: The effect of FGF7 on the ADAM17-EGFR-ERK1/2 signaling pathway in 16HBE cells. (A, B) Representative Western blots and densitometry for FGF7 and p-FGFR2/FGFR2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (C, D) Representative Western blots and densitometry for FGF7, ADAM17, p-p38/p38, and p-AKT/AKT under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (E, F) Representative Western blots and densitometry for ADAM17, p-EGFR/EGFR, and p-ERK1/2/ERK1/2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). Compared to Control, * P < 0.05; Compared to CSE, # P < 0.05; Compared to CSE+FGF7, & P < 0.05.

    Article Snippet: Antibodies used included β-actin (1:1000, 100166-MM10, Sino Biological); KGF (1:800-1:1000, ab131162, abcam); ADAM17 (1:800-1:1000, ab2051, abcam); p38 (1:1500-1:2500, ab170099, abcam); p-p38 (1:800-1:1000, ab47363, abcam); AKT (1:1000-1:1200, 4691S, CST); p-AKT (1:800-1:1000, ab192623, abcam); EGFR (1:1000, ab32077, abcam); p-EGFR (1:600-1:1000, 3777S, CST); ERK1/2 (1:1000, ab184699, abcam); p-ERK1/2 (1:800-1:1000, 9101S, CST); FGFR2 (1:1000, A19051, Abclonal); p-FGFR2 (1:500, PFGFR2-240AP, Thermo).

    Techniques: Western Blot, Control

    (A) Relative expression levels of miR-671-5p after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). (B) Relative Fgfr2 mRNA expression levels after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001.

    Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

    Article Title: Circular RNA circSmad4 controls pulmonary fibrosis

    doi: 10.4196/kjpp.25.123

    Figure Lengend Snippet: (A) Relative expression levels of miR-671-5p after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). (B) Relative Fgfr2 mRNA expression levels after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001.

    Article Snippet: FGFR2-IN-1 (HY-145230; MedChemExpress) was used as a selective FGFR2 inhibitor and dissolved in dimethyl sulfoxide to the desired concentrations.

    Techniques: Expressing

    (A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

    Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

    Article Title: Circular RNA circSmad4 controls pulmonary fibrosis

    doi: 10.4196/kjpp.25.123

    Figure Lengend Snippet: (A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

    Article Snippet: FGFR2-IN-1 (HY-145230; MedChemExpress) was used as a selective FGFR2 inhibitor and dissolved in dimethyl sulfoxide to the desired concentrations.

    Techniques: Transfection, Expressing

    (A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

    Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

    Article Title: Circular RNA circSmad4 controls pulmonary fibrosis

    doi: 10.4196/kjpp.25.123

    Figure Lengend Snippet: (A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

    Article Snippet: FGFR2-IN-1 (HY-145230; MedChemExpress) was used as a selective FGFR2 inhibitor and dissolved in dimethyl sulfoxide to the desired concentrations.

    Techniques: Transfection, Expressing