resource source identifier antibodies polyclonal rabbit anti focal adhesion kinase anti fak cell signaling technologies  (Cell Signaling Technology Inc)

Journal: Journal of Cell Science

Article Title: Apical-out polarity in epithelial spheroids requires α6β4 integrins, cell proliferation and anchorage independence

doi: 10.1242/jcs.264323

Figure Lengend Snippet: Anchorage independence is required for apical-out polarity. (A) MDCK cells were seeded into soft agar. Cells were left untreated or were treated with RhoA activator II. (B) Quantification of colonies formed in the agar assay. Each data point represents the mean (from a minimum of three field of view) from each experimental replicate (three replicate experiments were performed in total) (error bars are overall mean±s.d.). * P <0.05 (paired two-tailed t -test). (C) MDCK cysts were grown in Matrigel for 7 days and then treated with RhoA activator II for 72 h, pre-treated with FAK inhibitor Y15 24 h followed by Y15+Rho Activator II for an additional 48 h, or treated with Rho activator II for 24 h, followed by Y15+Rho activator II for an additional 48 h (post treatment). (D) Quantification of normal, disrupted lumen and eversion for each condition. Each data point represents the mean (expressed as a percentage) of each condition per replicate experiment (minimum of 10 cysts analyzed per condition per experiment, five replicate experiments performed in total; error bars are overall mean±s.d.). ** P <0.01; ns, not significant (two-way ANOVA with Tukey's multiple comparison test).

Article Snippet: Focal adhesion kinase (FAK) inhibitor Y15 (also known as FAK inhibitor 14) was used at a final concentration of 2.5 μM (Medchem express, catalog HY-12444).

Techniques: Two Tailed Test, Comparison

Journal: Translational Oncology

Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

doi: 10.1016/j.tranon.2026.102732

Figure Lengend Snippet: NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.

Article Snippet: GBM cells were treated with 10 μM focal adhesion kinase (FAK) activator Adhesamine (HY-122,672, MCE, USA) for 24 h, and the cells were divided into sh-NC group, sh-NRP2 group and sh-NRP2+Adhesamine group.

Techniques: Expressing, Knockdown, Quantitative RT-PCR, CCK-8 Assay, Migration, Double Staining, Western Blot

Journal: Translational Oncology

Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

doi: 10.1016/j.tranon.2026.102732

Figure Lengend Snippet: The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.

Article Snippet: GBM cells were treated with 10 μM focal adhesion kinase (FAK) activator Adhesamine (HY-122,672, MCE, USA) for 24 h, and the cells were divided into sh-NC group, sh-NRP2 group and sh-NRP2+Adhesamine group.

Techniques: Injection, Stable Transfection, Transfection, Comparison, Expressing

Journal: Biomolecules

Article Title: Halogen-Containing Drugs in 2025: A Record Year for the Therapeutic Use and Synthesis of FDA-Approved Small Molecules

doi: 10.3390/biom16030381

Figure Lengend Snippet: Structures of avutometinib ( 41 ) and defactinib ( 42 ).

Article Snippet: The ATP-competitive focal adhesion kinase (FAK) inhibitor defactinib, often referred to as VS-6063, was developed by Pfizer and is currently owned by Verastem [ ].

Techniques:

Journal: Biomolecules

Article Title: Halogen-Containing Drugs in 2025: A Record Year for the Therapeutic Use and Synthesis of FDA-Approved Small Molecules

doi: 10.3390/biom16030381

Figure Lengend Snippet: Preparation of defactinib ( 42 ).

Article Snippet: The ATP-competitive focal adhesion kinase (FAK) inhibitor defactinib, often referred to as VS-6063, was developed by Pfizer and is currently owned by Verastem [ ].

Techniques:

Journal: Biomolecules

Article Title: Halogen-Containing Drugs in 2025: A Record Year for the Therapeutic Use and Synthesis of FDA-Approved Small Molecules

doi: 10.3390/biom16030381

Figure Lengend Snippet: Experimental bound conformation of defactinib (PDB: 5MAH ; crystal structure of MELK in complex with defactinib). Defactinib is depicted as thick green sticks, MELK is represented by cyan cartoons and thin sticks. H-bonds are represented by yellow dashed lines.

Article Snippet: The ATP-competitive focal adhesion kinase (FAK) inhibitor defactinib, often referred to as VS-6063, was developed by Pfizer and is currently owned by Verastem [ ].

Techniques: