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p fgfr1 antibody  (Proteintech)


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    Structured Review

    Proteintech p fgfr1 antibody
    P Fgfr1 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 51 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p fgfr1 antibody/product/Proteintech
    Average 94 stars, based on 51 article reviews
    p fgfr1 antibody - by Bioz Stars, 2026-03
    94/100 stars

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    The molecular mechanism responsible for the synergistic effects of Erdafitinib and Stattic on H520 cells. A: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h) group and Control group. B: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h)+Stattic (Sta, 2.5 µM, 24 h) group and Control group. C: The concurrent effects of Erdafitinib (Erda,10 µM, 24 h) and Stattic (Sta, 2.5 µM, 24 h) on <t>FGFR1/STAT3</t> signaling in H520 cells. D: The concurrent effects of FGFR1 knockdown and Stattic (Sta, 2.5 µM) on FGFR1/STAT3 signaling in H520 cells. Data was expressed as mean ± SD of three experiments and each experiment included triplicate repeats. ** p <0.01 vs. Control, ## p <0.01 vs. Erda alone, && p <0.01 vs. Sta alone.
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    Proteintech p fgfr1
    The molecular mechanism responsible for the synergistic effects of Erdafitinib and Stattic on H520 cells. A: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h) group and Control group. B: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h)+Stattic (Sta, 2.5 µM, 24 h) group and Control group. C: The concurrent effects of Erdafitinib (Erda,10 µM, 24 h) and Stattic (Sta, 2.5 µM, 24 h) on <t>FGFR1/STAT3</t> signaling in H520 cells. D: The concurrent effects of FGFR1 knockdown and Stattic (Sta, 2.5 µM) on FGFR1/STAT3 signaling in H520 cells. Data was expressed as mean ± SD of three experiments and each experiment included triplicate repeats. ** p <0.01 vs. Control, ## p <0.01 vs. Erda alone, && p <0.01 vs. Sta alone.
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    Image Search Results


    The FGFR1-dependent pathway is a target of PM2.5 in non-small cell lung cancer H460 and A549 cells. (A-B) H460 cells were treated with PM2.5 of 0-200 μg/ml and (C-D) A549 cells were treated with PM2.5 of 0-100 μg/ml for 24 h. Then, the expression level of FGFR1 was determined by western blot analysis. β-actin was used as a loading control. The band intensities of the PM2.5 treatment groups were quantified by densitometry using ImageJ, and the results are presented as a relative protein level. (E-F) H460 cells and (G-H) A549 cells were treated with PM2.5 of 0-200 μg/ml for 24 h. The expression of FGFR1 was determined by immunofluorescence. The fluorescence intensity was analyzed by ImageJ, and the results are presented as relative protein intensity. Data are presented as mean±standard deviation (n=3). Multiple comparisons were conducted using one-way analysis of variance (ANOVA) followed by Turkey’s post hoc test and the statistical difference between the two groups was compared using t-test.*p<0.05 and **p<0.01 versus untreated control cells. PM2.5: Particulate matter 2.5.

    Journal: Cancer Genomics & Proteomics

    Article Title: Particulate Matter 2.5 Induces FGFR1-mediated Integrin Switch to Promote Non-small Cell Lung Cancer Metastasis

    doi: 10.21873/cgp.20527

    Figure Lengend Snippet: The FGFR1-dependent pathway is a target of PM2.5 in non-small cell lung cancer H460 and A549 cells. (A-B) H460 cells were treated with PM2.5 of 0-200 μg/ml and (C-D) A549 cells were treated with PM2.5 of 0-100 μg/ml for 24 h. Then, the expression level of FGFR1 was determined by western blot analysis. β-actin was used as a loading control. The band intensities of the PM2.5 treatment groups were quantified by densitometry using ImageJ, and the results are presented as a relative protein level. (E-F) H460 cells and (G-H) A549 cells were treated with PM2.5 of 0-200 μg/ml for 24 h. The expression of FGFR1 was determined by immunofluorescence. The fluorescence intensity was analyzed by ImageJ, and the results are presented as relative protein intensity. Data are presented as mean±standard deviation (n=3). Multiple comparisons were conducted using one-way analysis of variance (ANOVA) followed by Turkey’s post hoc test and the statistical difference between the two groups was compared using t-test.*p<0.05 and **p<0.01 versus untreated control cells. PM2.5: Particulate matter 2.5.

    Article Snippet: The membranes were blocked with 5% skimmed milk in TBST (25 mm Tris-HCl, pH 7.4, 125 mm NaCl, and 0.05% Tween 20) for 1 h. They were then incubated with the specific primary antibodies against FGFR1, integrin αV, integrin β1, Akt, p-Akt and β-actin (Cell Signaling, Danvers, MA, USA).

    Techniques: Expressing, Western Blot, Control, Immunofluorescence, Fluorescence, Standard Deviation

    PM2.5 induces the expression of proteins involved cell migration in non-small cell lung cancer H460 and A549 cells. (A-B) H460 cells were treated with PM2.5 of 0-200 μg/ml and (C-D) A549 cells were treated with PM2.5 of 0-100 μg/ml for 24 h. Then, the expression level of integrin αV, β1, Akt, and p-Akt determined by western blot analysis. β-actin was used as a loading control. The band intensities of the PM2.5 treatment groups were quantified by densitometry using ImageJ, and the results are presented as relative protein level. Data are presented as mean ± standard deviation (n=3). Multiple comparisons were conducted using one-way analysis of variance (ANOVA) followed by Turkey’s post hoc test.*p<0.05, **p<0.01, ***p<0.001 and ****p<0.0001 versus untreated control cells. PM2.5: Particulate matter 2.5.

    Journal: Cancer Genomics & Proteomics

    Article Title: Particulate Matter 2.5 Induces FGFR1-mediated Integrin Switch to Promote Non-small Cell Lung Cancer Metastasis

    doi: 10.21873/cgp.20527

    Figure Lengend Snippet: PM2.5 induces the expression of proteins involved cell migration in non-small cell lung cancer H460 and A549 cells. (A-B) H460 cells were treated with PM2.5 of 0-200 μg/ml and (C-D) A549 cells were treated with PM2.5 of 0-100 μg/ml for 24 h. Then, the expression level of integrin αV, β1, Akt, and p-Akt determined by western blot analysis. β-actin was used as a loading control. The band intensities of the PM2.5 treatment groups were quantified by densitometry using ImageJ, and the results are presented as relative protein level. Data are presented as mean ± standard deviation (n=3). Multiple comparisons were conducted using one-way analysis of variance (ANOVA) followed by Turkey’s post hoc test.*p<0.05, **p<0.01, ***p<0.001 and ****p<0.0001 versus untreated control cells. PM2.5: Particulate matter 2.5.

    Article Snippet: The membranes were blocked with 5% skimmed milk in TBST (25 mm Tris-HCl, pH 7.4, 125 mm NaCl, and 0.05% Tween 20) for 1 h. They were then incubated with the specific primary antibodies against FGFR1, integrin αV, integrin β1, Akt, p-Akt and β-actin (Cell Signaling, Danvers, MA, USA).

    Techniques: Expressing, Migration, Western Blot, Control, Standard Deviation

    Resource of antibodies.

    Journal: Cell Proliferation

    Article Title: Flavonoid chrysin activates both TrkB and FGFR1 receptors while upregulates their endogenous ligands such as brain derived neurotrophic factor to promote human neurogenesis

    doi: 10.1111/cpr.13732

    Figure Lengend Snippet: Resource of antibodies.

    Article Snippet: Rabbit anti p‐FGFR1 , CST , Ab173305.

    Techniques:

    The molecular mechanism responsible for the synergistic effects of Erdafitinib and Stattic on H520 cells. A: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h) group and Control group. B: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h)+Stattic (Sta, 2.5 µM, 24 h) group and Control group. C: The concurrent effects of Erdafitinib (Erda,10 µM, 24 h) and Stattic (Sta, 2.5 µM, 24 h) on FGFR1/STAT3 signaling in H520 cells. D: The concurrent effects of FGFR1 knockdown and Stattic (Sta, 2.5 µM) on FGFR1/STAT3 signaling in H520 cells. Data was expressed as mean ± SD of three experiments and each experiment included triplicate repeats. ** p <0.01 vs. Control, ## p <0.01 vs. Erda alone, && p <0.01 vs. Sta alone.

    Journal: Journal of Cancer

    Article Title: STAT3 inhibitor Stattic Exhibits the Synergistic Effect with FGFRs Inhibitor Erdafitinib in FGFR1-positive Lung Squamous Cell Carcinoma

    doi: 10.7150/jca.97477

    Figure Lengend Snippet: The molecular mechanism responsible for the synergistic effects of Erdafitinib and Stattic on H520 cells. A: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h) group and Control group. B: Analysis of Volcano plots, GO pathway and KEGG pathway between the Erdafitinib (Erda,10 µM, 24 h)+Stattic (Sta, 2.5 µM, 24 h) group and Control group. C: The concurrent effects of Erdafitinib (Erda,10 µM, 24 h) and Stattic (Sta, 2.5 µM, 24 h) on FGFR1/STAT3 signaling in H520 cells. D: The concurrent effects of FGFR1 knockdown and Stattic (Sta, 2.5 µM) on FGFR1/STAT3 signaling in H520 cells. Data was expressed as mean ± SD of three experiments and each experiment included triplicate repeats. ** p <0.01 vs. Control, ## p <0.01 vs. Erda alone, && p <0.01 vs. Sta alone.

    Article Snippet: Reagents such as antibodies were used as follows: FGFR1 (1:500, ab76464, Abcam, MA, USA), p-FGFR1 (1:1000, ab173305, Abcam), FGFR2 (1:1000, ab109372, Abcam), p-FGFR2 (1:2000, abs140266, Absin, Shanghai, China), FGFR3 (1:2000, ab133644, Abcam), p-FGFR3 (1:200, abs140268, Absin), FGFR4 (1:1000, ab178396, Abcam), p-FGFR4 (1:2000, abs1039979, Absin), AKT (1:1000, ab185633, Abcam), p-AKT (1:1000, ab192623, Abcam), ERK1/2 (1:1000, AF1051, Beyotime, Nantong, China), p-ERK1/2 (1:1000, AF1891, Beyotime), STAT3 (1:1000, ab68153, Abcam), p-STAT3 (1:1000, ab267373, Abcam), E-Cadherin (1:1000, sc-8426, Santa Cruz Biotechnology, CA, USA), Vimentin (1:1000, sc-373717, Santa Cruz Biotechnology), GAPDH (1:2000, D190090, Sangon Biotech, Shanghai, China), HRP-labeled Goat Anti-Mouse IgG(H+L) (1:1000, A0216, Beyotime), HRP-labeled Goat Anti-Rabbit IgG(H+L) (1:1000, A0208, Beyotime).

    Techniques: Control, Knockdown

    The synergistic effects of Erdafitinib and Stattic against tumorigenesis in vivo . H520 xenograft model was constructed and treated with Erdafitinib (Erda, 10 mg/kg/day), Stattic (Sta, 5 mg/kg/day), or their combination (10 mg/kg/day Erdafitinib, 5 mg/kg/day Stattic) for 2 weeks. A: Tumor volumes were measured every other day. B: Body weights were measured every other day. C&D: MicroPET was conducted using 18 F-FDG. E: Representative images of hematoxylin-eosin (H&E), TUNEL, Ki67 and FGFR1/pSTAT3 staining in H520 xenografts. Data was expressed as mean ± SD of three experiments and each experiment included triplicate repeats. ** p <0.01 vs. Control, ## p <0.01 vs. Erda alone, && p <0.01 vs. Sta alone.

    Journal: Journal of Cancer

    Article Title: STAT3 inhibitor Stattic Exhibits the Synergistic Effect with FGFRs Inhibitor Erdafitinib in FGFR1-positive Lung Squamous Cell Carcinoma

    doi: 10.7150/jca.97477

    Figure Lengend Snippet: The synergistic effects of Erdafitinib and Stattic against tumorigenesis in vivo . H520 xenograft model was constructed and treated with Erdafitinib (Erda, 10 mg/kg/day), Stattic (Sta, 5 mg/kg/day), or their combination (10 mg/kg/day Erdafitinib, 5 mg/kg/day Stattic) for 2 weeks. A: Tumor volumes were measured every other day. B: Body weights were measured every other day. C&D: MicroPET was conducted using 18 F-FDG. E: Representative images of hematoxylin-eosin (H&E), TUNEL, Ki67 and FGFR1/pSTAT3 staining in H520 xenografts. Data was expressed as mean ± SD of three experiments and each experiment included triplicate repeats. ** p <0.01 vs. Control, ## p <0.01 vs. Erda alone, && p <0.01 vs. Sta alone.

    Article Snippet: Reagents such as antibodies were used as follows: FGFR1 (1:500, ab76464, Abcam, MA, USA), p-FGFR1 (1:1000, ab173305, Abcam), FGFR2 (1:1000, ab109372, Abcam), p-FGFR2 (1:2000, abs140266, Absin, Shanghai, China), FGFR3 (1:2000, ab133644, Abcam), p-FGFR3 (1:200, abs140268, Absin), FGFR4 (1:1000, ab178396, Abcam), p-FGFR4 (1:2000, abs1039979, Absin), AKT (1:1000, ab185633, Abcam), p-AKT (1:1000, ab192623, Abcam), ERK1/2 (1:1000, AF1051, Beyotime, Nantong, China), p-ERK1/2 (1:1000, AF1891, Beyotime), STAT3 (1:1000, ab68153, Abcam), p-STAT3 (1:1000, ab267373, Abcam), E-Cadherin (1:1000, sc-8426, Santa Cruz Biotechnology, CA, USA), Vimentin (1:1000, sc-373717, Santa Cruz Biotechnology), GAPDH (1:2000, D190090, Sangon Biotech, Shanghai, China), HRP-labeled Goat Anti-Mouse IgG(H+L) (1:1000, A0216, Beyotime), HRP-labeled Goat Anti-Rabbit IgG(H+L) (1:1000, A0208, Beyotime).

    Techniques: In Vivo, Construct, TUNEL Assay, Staining, Control