ArticleThe Journal of cell biology2006
An inhibitory role for FAK in regulating proliferation: a link between limited adhesion and RhoA-ROCK signaling.
Article in The Journal of cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
89 citing papers in PubMed, 187 citations in OpenAlex.
- Article
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- Replication of natural surface topographies to generate advanced cell culture substrates.Bioactive materials · 2023Review
- Effects of Nitro-Oxidative Stress on Biomolecules: Part 1-Non-Reactive Molecular Dynamics Simulations.Biomolecules · 2023Review
- The Effects of Different Doses of ROCK Inhibitor, Antifreeze Protein III, and Boron Added to Semen Extender on Semen Freezeability of Ankara Bucks.Molecules (Basel, Switzerland) · 2022Article
- In vivo dissection of Rhoa function in vascular development using zebrafish.Angiogenesis · 2022Article
- Generation, Transmission, and Regulation of Mechanical Forces in Embryonic Morphogenesis.Small (Weinheim an der Bergstrasse, Germany) · 2022Review
- Generation and Characterization of a Skeletal Muscle Cell-Based Model Carrying One Single Gne Allele: Implications in Actin Dynamics.Molecular neurobiology · 2021Article
- FAK Shutdown: Consequences on Epithelial Morphogenesis and Biomarker Expression Involving an Innovative Biomaterial for Tissue Regeneration.International journal of molecular sciences · 2021Article
- A novel lncRNA promotes myogenesis of bovine skeletal muscle satellite cells via PFN1-RhoA/Rac1.Journal of cellular and molecular medicine · 2021Article
- The role of Rho-associated kinase inhibitor, Y-27632 on primary culture of ovine spermatogonial stem cells.Animal reproduction · 2021Article
- Physical traits of cancer.Science (New York, N.Y.) · 2020Review
- A Hydrogel-Integrated Culture Device to Interrogate T Cell Activation with Physicochemical Cues.ACS applied materials & interfaces · 2020Article
- Acute compressive stress activates RHO/ROCK-mediated cellular processes.Small GTPases · 2020Article
- Feeling Things Out: Bidirectional Signaling of the Cell-ECM Interface, Implications in the Mechanobiology of Cell Spreading, Migration, Proliferation, and Differentiation.Advanced healthcare materials · 2020Review
- Review
- Intrinsic Cellular Responses of Human Wharton's Jelly Mesenchymal Stem Cells Influenced by OJournal of functional biomaterials · 2019Article
- Insulin Stimulates PI3K/AKT and Cell Adhesion to Promote the Survival of Individualized Human Embryonic Stem Cells.Stem cells (Dayton, Ohio) · 2019Article
29 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
Focal adhesion kinase (FAK) transduces cell adhesion to the extracellular matrix into proliferative signals. We show that FAK overexpression induced proliferation in endothelial cells, which are normally growth arrested by limited adhesion. Interestingly, displacement of FAK from adhesions by using a FAK-/- cell line or by expressing the C-terminal fragment FRNK also caused an escape of adhesion-regulated growth arrest, suggesting dual positive and negative roles for FAK in growth regulation. Expressing kinase-dead FAK-Y397F in FAK-/- cells prevented uncontrolled growth, demonstrating the antiproliferative function of inactive FAK. Unlike FAK overexpression-induced growth, loss of growth control in FAK-/- or FRNK-expressing cells increased RhoA activity, cytoskeletal tension, and focal adhesion formation. ROCK inhibition rescued adhesion-dependent growth control in these cells, and expression of constitutively active RhoA or ROCK dysregulated growth. These findings demonstrate the ability of FAK to suppress and promote growth, and underscore the importance of multiple mechanisms, even from one molecule, to control cell proliferation.
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What OpenQuestion holds
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.