ArticleMolecular and cellular biology2004
Focal adhesion kinase suppresses apoptosis by binding to the death domain of receptor-interacting protein.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 182 citations in OpenAlex.
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Transfer learning with multiomics integration and deep neural networks reveals drug resistance mechanisms in cancer.Scientific reports · 2025Article
- Inhibiting fibronectin assembly in the breast tumor microenvironment increases cell death and improves response to doxorubicin.bioRxiv : the preprint server for biology · 2025Article
- Dominant suppressor genes of p53-induced apoptosis in Drosophila melanogaster.G3 (Bethesda, Md.) · 2024Article
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- On the Value of In Vitro Cell Systems for Mechanobiology from the Perspective of Yes-Associated Protein/Transcriptional Co-Activator with a PDZ-Binding Motif and Focal Adhesion Kinase and Their Involvement in Wound Healing, Cancer, Aging, and Senescence.International journal of molecular sciences · 2023Review
- Mechanisms Underlying Anti-Inflammatory and Anti-Cancer Properties of Stretching-A Review.International journal of molecular sciences · 2022Review
- Cell adhesion tunes inflammatory TPL2 kinase signal transduction.Cellular and molecular life sciences : CMLS · 2022Article
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Focal adhesion kinase plays a dual role in TRAIL resistance and metastatic outgrowth of malignant melanoma.Cell death & disease · 2022Article
- Strong Binding of Phytochemicals to the Catalytic Domain of Tyrosine Hydroxylase as a Trojan Horse Decreases Dopamine in Dopaminergic Cells: Pharmaceutical Considerations in Schizophrenia and Parkinson's Disease.Current pharmaceutical design · 2022Article
- Functional and clinical characteristics of focal adhesion kinases in cancer progression.Frontiers in cell and developmental biology · 2022Review
- FAK inhibitors as promising anticancer targets: present and future directions.Future medicinal chemistry · 2021Review
- Cytotoxic and apoptosis-inducing effects of novel 8-amido isocoumarin derivatives against breast cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Review
- Article
- Radiosensitization by Kinase Inhibition Revealed by Phosphoproteomic Analysis of Pancreatic Cancer Cells.Molecular & cellular proteomics : MCP · 2020Article
- Therapeutic monoclonal antibody targeting of neuronal pentraxin receptor to control metastasis in gastric cancer.Molecular cancer · 2020Article
- Mechano-therapeutics: Targeting Mechanical Signaling in Fibrosis and Tumor Stroma.Pharmacology & therapeutics · 2020Review
- Development of a High-Throughput Fluorescence Polarization Assay to Detect Inhibitors of the FAK-Paxillin Interaction.SLAS discovery : advancing life sciences R & D · 2020Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Tumor cells resist the apoptotic stimuli associated with invasion and metastasis by activating survival signals that suppress apoptosis. Focal adhesion kinase (FAK), a tyrosine kinase that is overexpressed in a variety of human tumors, mediates one of these survival signals. Attenuation of FAK expression in tumor cells results in apoptosis that is mediated by caspase 8- and FADD-dependent pathways, suggesting that death receptor pathways are involved in the process. Here, we report a functional link between FAK and death receptors. We have demonstrated that FAK binds to the death domain kinase receptor-interacting protein (RIP). RIP is a major component of the death receptor complex and has been shown to interact with Fas and tumor necrosis factor receptor 1 through its binding to adapter proteins. We have shown that RIP provides proapoptotic signals that are suppressed by its binding to FAK. We thus propose that FAK overexpression in human tumors provides a survival signal function by binding to RIP and inhibiting its interaction with the death receptor complex.
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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.