ArticleMolecular cell2008
Nuclear FAK promotes cell proliferation and survival through FERM-enhanced p53 degradation.
Article in Molecular cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
291 citing papers in PubMed, 1 synthesis or guideline pooled it, 471 citations in OpenAlex.
- The effects of flavonoid baicalein on miRNA expressions in cancer: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Pooled it
- Irisin promotes lipid clearance through the CD81-integrin-FAK axis in steatotic hepatocytes.Journal of physiology and biochemistry · 2026Article
- Hypoxia-activated PROTAC for dual inhibition of FAK and EGFR enables synergistic mechano-chemical cancer therapy.Neoplasia (New York, N.Y.) · 2026Article
- Role of Focal Adhesion Kinase and NRF2 Pathways in Gastrointestinal Wound Healing.International journal of molecular sciences · 2026Review
- Mechanoresponsive modulation of nuclear pore complex structure and function bybioRxiv : the preprint server for biology · 2026Article
- Glutamate-induced nuclear translocation of PYK2 in hippocampal neurons, interaction with MBD2, and role in cell death in a model of epilepsy.Cell death & disease · 2026Article
- Review
- Inactivation of Focal Adhesion Kinase FAK Rapidly Abrogates Keratinocyte Entry in Mitosis via Rho-Associated Kinase, Resulting in Squamous Differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- Strategic selection of MDM2 inhibitors enhances the efficacy of FAK inhibition in mesothelioma based on TP53 genotype.PloS one · 2026Article
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Targeting PTK2 by vaccarin alleviates osteoporosis through inhibiting ferroptosis via modulating P53 acetylation/succinylation.Cell biology and toxicology · 2025Article
- 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
- Immunotyping of thyroid cancer for clinical outcomes and implications.Cancer immunology, immunotherapy : CII · 2025Article
- Targeting the hydrophobic pockets of FAK/PYK2 FAT domain: a highly effective inhibitory strategy suppressing tumor growth and eliminating metastasis.Cell communication and signaling : CCS · 2025Article
- Article
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Pyrimidine: A Privileged Scaffold for the Development of Anticancer Agents as Protein Kinase Inhibitors (Recent Update).Current pharmaceutical design · 2025Review
- Recent Prospectives of Cellular Signaling Role for Mammary Gland Carcinogenesis.Anti-cancer agents in medicinal chemistry · 2025Review
- Focal adhesion kinase promotes ribosome biogenesis to drive advanced thyroid cancer cell growth and survival.Frontiers in oncology · 2025Article
231 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
FAK is known as an integrin- and growth factor-associated tyrosine kinase promoting cell motility. Here we show that, during mouse development, FAK inactivation results in p53- and p21-dependent mesodermal cell growth arrest. Reconstitution of primary FAK-/-p21-/- fibroblasts revealed that FAK, in a kinase-independent manner, facilitates p53 turnover via enhanced Mdm2-dependent p53 ubiquitination. p53 inactivation by FAK required FAK FERM F1 lobe binding to p53, FERM F2 lobe-mediated nuclear localization, and FERM F3 lobe for connections to Mdm2 and proteasomal degradation. Staurosporine or loss of cell adhesion enhanced FERM-dependent FAK nuclear accumulation. In primary human cells, FAK knockdown raised p53-p21 levels and slowed cell proliferation but did not cause apoptosis. Notably, FAK knockdown plus cisplatin triggered p53-dependent cell apoptosis, which was rescued by either full-length FAK or FAK FERM re-expression. These studies define a scaffolding role for nuclear FAK in facilitating cell survival through enhanced p53 degradation under conditions of cellular stress.
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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.