fak antibody  (Santa Cruz Biotechnology)

Journal: Bioactive Materials

Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

doi: 10.1016/j.bioactmat.2026.01.046

Figure Lengend Snippet: Immunofluorescence staining of focal adhesion-related markers and cytoskeleton in cells under control and mechanical stimulation conditions. Left (Control group): Immunofluorescence staining shows focal adhesion-associated proteins (green channels). These correspond to integrin β1(A), talin (B), pFAK/FAK (C), paxillin (D), YAP (E), and TAZ (F) in each row. F-actin and FAK are shown in the red channel. The rightmost column of each row displays merged images. These integrate focal adhesion marker signals (green), F-actin (red), and DAPI-stained nuclei (blue). Yellow indicates co-localization of focal adhesion markers and F-actin. Right (After mechanical stimulation group): Immunofluorescence staining displays the same set of focal adhesion-related proteins and F-actin in cells after mechanical stimulation. Merged images are presented in the same format as the control group.

Article Snippet: FAK Antibody (sc-271126), pFAK(Y3978556s), talin (sc: 4021s), paxillin (sc: 365379), integrin β1 (sc: 374429), and YAP (cst: 14074s), TAZ (cst: 83669s) were ordered from Santa Cruz Biotechnology.

Techniques: Immunofluorescence, Staining, Control, Marker

Journal: Molecular Biomedicine

Article Title: RPRD1A drives lenvatinib resistance in hepatocellular carcinoma via the ITGA5-FAK signaling axis

doi: 10.1186/s43556-026-00459-8

Figure Lengend Snippet: ITGA5 induces resistance to lenvatinib in RPRD1A-overexpressing HCC cells through the FAK pathway. a Heatmap showing phosphorylated protein differential expression between PLC-LV-RPRD1A and PLC-VECTOR cells. b Expression of phosphorylated FAK protein in PLC-LV-RPRD1A (left panel) and Huh7-LV-RPRD1A (right panel) cells via western blot analysis. c Expression of phosphorylated FAK protein in siITGA5-transfected PLC-LV-RPRD1A (left panel), Huh7-LV-RPRD1A (right panel), and their control cells via western blot analysis. d Representative images and statistical analysis of IHC staining of RPRD1A, ITGA5 and FAK in PLC-LV-RPRD1A and PLC-VECTOR mice tumors (n = 6), scale bar: 200 μm. e Time-course survival rates of PLC-LV-RPRD1A (left panel) and Huh7-LV-RPRD1A (right panel) cells treated with lenvatinib (30 μM), Donafenib (5 μM), their single-agent controls or the combination therapy, assessed at 24-h intervals over a 4-day period (n = 3). f Time-course survival rates of PLC-LV-RPRD1A (left panel) and Huh7-LV-RPRD1A (right panel) cells treated with lenvatinib (30 μM), Volociximab (100 nM), their single-agent controls or the combination therapy, assessed at 24-h intervals over a 4-day period (n = 3). g Experimental design of the treatment procedure. h Photographs of tumors of mice in the xenograft models (C57BL/6 mice bearing H22-LV-RPRD1A subcutaneous xenografts after treatment with PBS, lenvatinib (30 mg/kg), Donafenib (50 mg/kg), Volociximab (10 mg/kg), or their combinations) are shown (n = 4). i Tumor volumes of mice in the xenograft models in ( h ) are shown (n = 4). Data are presented as mean ± SEM, statistical significance: ns. not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Article Snippet: Membranes were blocked with 5% BSA (#ST023, Beyotime) (1 h, RT) then incubated overnight at 4 °C with primary antibodies diluted in Primary Antibody Dilution Buffer solution (#P0023A, Beyotime): β-actin (1:5000; #66,009–1-Ig; Proteintech), IgG isotype control (1:1000; #sc-66931; Santa Cruz), RPRD1A (1:1000; #23,652–1-AP; Proteintech), ITGA5 (1:1000; #ab150361; Abcam), FAK (1:500; #HY-P80125; MCE), p-FAK [Tyr397] (1:1000; #3283S; CST), AKT (1:1000; #9272; CST), p-AKT [Ser473] (1:1000; #9271; CST), ERK (1:1000; #4695; MCE), p-ERK [Thr202/Tyr204] (1:1000; #4370; CST), RPAP2 (1:1000; #17,401–1-AP; Proteintech), RPB1 (1:1000; #14958S; CST), and c-JUN (1:1000; #9165T; CST).

Techniques: Quantitative Proteomics, Plasmid Preparation, Expressing, Western Blot, Transfection, Control, Immunohistochemistry

Journal: Molecular Biomedicine

Article Title: RPRD1A drives lenvatinib resistance in hepatocellular carcinoma via the ITGA5-FAK signaling axis

doi: 10.1186/s43556-026-00459-8

Figure Lengend Snippet: Rescue experiments confirm the RPRD1A–ITGA5–FAK axis in mediating lenvatinib resistance. a Dose–response curves and IC50 values of lenvatinib in PLC/PRF/5 cells co-transfected with RPRD1A siRNA and ITGA5 overexpression plasmid or control constructs, following 48 h treatment (n = 3). b Representative images and statistical analysis of long-term colony formation assay of RPRD1A-knockdown and ITGA5 overexpression PLC-LV-RPRD1A and their control cells. Cells were grown in the presence of lenvatinib at the indicated concentrations for 14 days (n = 3). c Dose–response curves and IC50 values of lenvatinib in PLC‑LV‑RPRD1A cells co-transfected with ITGA5 siRNA and CA-FAK or control FAK plasmid, following 48 h treatment (n = 3). d Representative images and statistical analysis of long-term colony formation assay of ITGA5-knockdown and FAK overexpression PLC-LV-RPRD1A and their control cells. Cells were grown in the presence of lenvatinib at the indicated concentrations for 14 days (n = 3). Data are presented as mean ± SEM, statistical significance: ns. not significant, *** p < 0.001, and **** p < 0.0001

Article Snippet: Membranes were blocked with 5% BSA (#ST023, Beyotime) (1 h, RT) then incubated overnight at 4 °C with primary antibodies diluted in Primary Antibody Dilution Buffer solution (#P0023A, Beyotime): β-actin (1:5000; #66,009–1-Ig; Proteintech), IgG isotype control (1:1000; #sc-66931; Santa Cruz), RPRD1A (1:1000; #23,652–1-AP; Proteintech), ITGA5 (1:1000; #ab150361; Abcam), FAK (1:500; #HY-P80125; MCE), p-FAK [Tyr397] (1:1000; #3283S; CST), AKT (1:1000; #9272; CST), p-AKT [Ser473] (1:1000; #9271; CST), ERK (1:1000; #4695; MCE), p-ERK [Thr202/Tyr204] (1:1000; #4370; CST), RPAP2 (1:1000; #17,401–1-AP; Proteintech), RPB1 (1:1000; #14958S; CST), and c-JUN (1:1000; #9165T; CST).

Techniques: Transfection, Over Expression, Plasmid Preparation, Control, Construct, Colony Assay, Knockdown

Journal: Molecular Biomedicine

Article Title: RPRD1A drives lenvatinib resistance in hepatocellular carcinoma via the ITGA5-FAK signaling axis

doi: 10.1186/s43556-026-00459-8

Figure Lengend Snippet: RPRD1A and ITGA5 expression levels correlate with lenvatinib clinical responsiveness. a Representative images and statistical analysis of IHC staining of RPRD1A expression in HCC tissues from clinically lenvatinib-sensitive and lenvatinib-resistant patients, scale bar, 200 μm. b Survival analysis of RPRD1A expression levels and prognosis in HCC based on data from the GEPIA2.0 database. c Representative images and statistical analysis of IHC staining of ITGA5 expression in HCC tissues from clinically lenvatinib-sensitive and lenvatinib-resistant patients, scale bar, 200 μm. d Survival analysis of ITGA5 expression levels and prognosis in HCC based on data from the GEPIA2.0 database. e Kaplan–Meier analysis of lenvatinib sensitivity and RFS in HCC patients. f Kaplan–Meier analysis of RPRD1A expression and RFS in HCC patients. g Kaplan–Meier analysis of ITGA5 expression and RFS in HCC patients. h Schematic overview of the present study: RPRD1A positively regulates ITGA5 expression by competitively binding to RNA Pol II and interfering with RPAP2, leading to activation of the focal adhesion kinase (FAK) signaling pathway and subsequent non-canonical induction of lenvatinib resistance

Article Snippet: Membranes were blocked with 5% BSA (#ST023, Beyotime) (1 h, RT) then incubated overnight at 4 °C with primary antibodies diluted in Primary Antibody Dilution Buffer solution (#P0023A, Beyotime): β-actin (1:5000; #66,009–1-Ig; Proteintech), IgG isotype control (1:1000; #sc-66931; Santa Cruz), RPRD1A (1:1000; #23,652–1-AP; Proteintech), ITGA5 (1:1000; #ab150361; Abcam), FAK (1:500; #HY-P80125; MCE), p-FAK [Tyr397] (1:1000; #3283S; CST), AKT (1:1000; #9272; CST), p-AKT [Ser473] (1:1000; #9271; CST), ERK (1:1000; #4695; MCE), p-ERK [Thr202/Tyr204] (1:1000; #4370; CST), RPAP2 (1:1000; #17,401–1-AP; Proteintech), RPB1 (1:1000; #14958S; CST), and c-JUN (1:1000; #9165T; CST).

Techniques: Expressing, Immunohistochemistry, Binding Assay, Activation Assay