ArticleScience signaling2014
A FAK-Cas-Rac-lamellipodin signaling module transduces extracellular matrix stiffness into mechanosensitive cell cycling.
Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
120 citing papers in PubMed, 232 citations in OpenAlex.
- Article
- Activation of the FAK-MAPK/ERK1 pathway promotes intestinal epithelial cell sheet migration during fistula tract repair.Scientific reports · 2026Article
- Extracellular matrix stiffness determines the phenotypic behavior of dedifferentiated melanoma cells through a DDR1/2-dependent YAP mechanotransduction pathway.Oncogenesis · 2026Article
- Mechanotherapeutic Potential of Survivin in Glioblastoma.bioRxiv : the preprint server for biology · 2026Article
- Cancer cells metastasize in several types of cancer via two distinct routes, probably based on mechanical signals.Frontiers in cell and developmental biology · 2026Review
- Review
- An overview of mechanical microenvironment and mechanotransduction in intervertebral disc degeneration.Experimental & molecular medicine · 2025Review
- Mechanosensitive biochemical imprinting of the talin interaction with DLC1 regulates RhoA activity and cardiomyocyte remodeling.Science advances · 2025Article
- Matrix metalloproteinase-3 promotes arteriovenous fistula failure by regulating FAK-AKT signaling.bioRxiv : the preprint server for biology · 2025Article
- Survivin modulates stiffness-induced vascular smooth muscle cell motility.APL bioengineering · 2025Article
- Transcriptomic and Multi-scale Network Analyses Reveal Key Drivers of Cardiovascular Disease.IEEE transactions on molecular, biological, and multi-scale communications · 2025Article
- FAK and p130Cas Modulate Stiffness-Mediated Early Transcription and Cellular Metabolism.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Cancer-associated fibroblasts in clear cell renal cell carcinoma: functional heterogeneity, tumor microenvironment crosstalk, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Focal adhesion kinase signaling - tumor vulnerabilities and clinical opportunities.Journal of cell science · 2024Review
- A Hierarchical Mechanotransduction System: From Macro to Micro.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- FAK and p130Cas modulate stiffness-mediated early transcription and cellular metabolism.bioRxiv : the preprint server for biology · 2024Article
- FAK Family Kinases: A Potential Therapeutic Target for Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Arterial Mechanics, Extracellular Matrix, and Smooth Muscle Differentiation in Carotid Arteries Deficient for Rac1.Annals of vascular medicine and research · 2024Article
- Survivin as a mediator of stiffness-induced cell cycle progression and proliferation of vascular smooth muscle cells.APL bioengineering · 2023Article
- Survivin regulates intracellular stiffness and extracellular matrix production in vascular smooth muscle cells.APL bioengineering · 2023Article
60 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
9 authors at 1 institution in 1 country.
Funding
Abstract
Tissue and extracellular matrix (ECM) stiffness is transduced into intracellular stiffness, signaling, and changes in cellular behavior. Integrins and several of their associated focal adhesion proteins have been implicated in sensing ECM stiffness. We investigated how an initial sensing event is translated into intracellular stiffness and a biologically interpretable signal. We found that a pathway consisting of focal adhesion kinase (FAK), the adaptor protein p130Cas (Cas), and the guanosine triphosphatase Rac selectively transduced ECM stiffness into stable intracellular stiffness, increased the abundance of the cell cycle protein cyclin D1, and promoted S-phase entry. Rac-dependent intracellular stiffening involved its binding partner lamellipodin, a protein that transmits Rac signals to the cytoskeleton during cell migration. Our findings establish that mechanotransduction by a FAK-Cas-Rac-lamellipodin signaling module converts the external information encoded by ECM stiffness into stable intracellular stiffness and mechanosensitive cell cycling. Thus, lamellipodin is important not only in controlling cellular migration but also for regulating the cell cycle in response to mechanical signals.
Indexed as
Identifiers
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.