ArticleThe Journal of biological chemistry2010
Knock-in mutation reveals an essential role for focal adhesion kinase activity in blood vessel morphogenesis and cell motility-polarity but not cell proliferation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 113 citations in OpenAlex.
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- FAK inhibition in ovarian cancer releases omega-3 fatty acids to program CXCL13-producing anti-tumor resident peritoneal macrophages.Cell reports · 2026Article
- Designing novel FAK inhibitors targeting gastric cancer: a combined approach using machine learning, docking analysis, molecular dynamics simulations, and experimental validation.Journal of computer-aided molecular design · 2026Article
- Focal adhesion kinase inhibition induces membrane accumulation of aquaporin-2 in renal epithelial cells by actin depolymerization and endocytosis inhibition.American journal of physiology. Renal physiology · 2025Article
- Ovarian Tumor FAK Inhibition Releases Omega-3 Fatty Acids Stimulating GATA6 Peritoneal Macrophage CXCL13 Production Enhancing Immunotherapy.bioRxiv : the preprint server for biology · 2025Article
- Feto-placental blood vessel development.Development (Cambridge, England) · 2025Review
- Inducible FAK loss but not FAK inhibition in endothelial cells of PYK2-null mice activates p53 tumor suppressor to prevent tumor growth.Molecular biology of the cell · 2025Article
- FAK inhibition disrupts tumor growth, apoptosis, and transcriptional regulation in GI-NETs.Endocrine oncology (Bristol, England) · 2025Article
- Focal adhesion kinase promotes ribosome biogenesis to drive advanced thyroid cancer cell growth and survival.Frontiers in oncology · 2025Article
- Clinic Examination and Gene Diagnosis for a Birt-Hogg-Dubé Syndrome Family With a NovelHuman mutation · 2025Article
- Targeting FAK to Potentiate Immune Checkpoint Therapy in Solid Tumors.Journal of cancer immunology · 2025Article
- Focal adhesion kinase signaling - tumor vulnerabilities and clinical opportunities.Journal of cell science · 2024Review
- FAK, vinculin, and talin control mechanosensitive YAP nuclear localization.Biomaterials · 2024Article
- Focal adhesion kinase confers lenvatinib resistance in hepatocellular carcinoma via the regulation of lysine-deficient kinase 1.Molecular carcinogenesis · 2024Article
- Nuclear FAK in endothelium: An intrinsic inhibitor of NF-κB activation in atherosclerosis.Atherosclerosis · 2023Article
- Focal adhesion kinase-mediated signaling controls the onset of pancreatic cell differentiation.Development (Cambridge, England) · 2022Article
- ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning.Development (Cambridge, England) · 2022Article
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Phosphorylation of pericyte FAK-Y861 affects tumour cell apoptosis and tumour blood vessel regression.Angiogenesis · 2021Article
- Focal Adhesion Kinase Activity and Localization is Critical for TNF-α-Induced Nuclear Factor-κB Activation.Inflammation · 2021Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Focal adhesion kinase (FAK) associates with both integrins and growth factor receptors in the control of cell motility and survival. Loss of FAK during mouse development results in lethality at embryonic day 8.5 (E8.5) and a block in cell proliferation. Because FAK serves as both a scaffold and signaling protein, gene knock-outs do not provide mechanistic insights in distinguishing between these modes of FAK function. To determine the role of FAK activity during development, a knock-in point mutation (lysine 454 to arginine (R454)) within the catalytic domain was introduced by homologous recombination. Homozygous FAK(R454/R454) mutation was lethal at E9.5 with defects in blood vessel formation as determined by lack of yolk sac primary capillary plexus formation and disorganized endothelial cell patterning in FAK(R454/R454) embryos. In contrast to the inability of embryonic FAK(-/-) cells to proliferate ex vivo, primary FAK(R454/R454) mouse embryo fibroblasts (MEFs) were established from E8.5 embryos. R454 MEFs exhibited no difference in cell growth compared with normal MEFs, and R454 FAK localized to focal adhesions but was not phosphorylated at Tyr-397. In E8.5 embryos and primary MEFs, FAK R454 mutation resulted in decreased c-Src Tyr-416 phosphorylation. R454 MEFs exhibited enhanced focal adhesion formation, decreased migration, and defects in cell polarity. Within immortalized MEFs, FAK activity was required for fibronectin-stimulated FAK-p190RhoGAP association and p190RhoGAP tyrosine phosphorylation linked to decreased RhoA GTPase activity, focal adhesion turnover, and directional motility. Our results establish that intrinsic FAK activity is essential for developmental processes controlling blood vessel formation and cell motility-polarity but not cell proliferation. This work supports the use of FAK inhibitors to disrupt neovascularization.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.