ArticlePloS one2013
The RhoGEF TEM4 Regulates Endothelial Cell Migration by Suppressing Actomyosin Contractility.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Contractile forces direct the chiral swirling of minimal cell collectives.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dynamic decoding of VEGF signaling and coordinated control of multiple phenotypes by the Src-TEM4-YAP pathway.Cell systems · 2025Article
- ARHGEF17/TEM4 regulates the cell cycle through control of G1 progression.The Journal of cell biology · 2025Article
- A commercial ARHGEF17/TEM4 antibody cross-reacts with Nuclear Mitotic Apparatus protein 1 (NuMA).PloS one · 2022Article
- Role of RhoC in cancer cell migration.Cancer cell international · 2021Review
- Copy number aberrations drive kinase rewiring, leading to genetic vulnerabilities in cancer.Cell reports · 2021Article
- Article
- cAMP guided his way: a life for G protein-mediated signal transduction and molecular pharmacology-tribute to Karl H. Jakobs.Naunyn-Schmiedeberg's archives of pharmacology · 2019Review
- ARHGAP18: A Flow-Responsive Gene That Regulates Endothelial Cell Alignment and Protects Against Atherosclerosis.Journal of the American Heart Association · 2019Article
- Biomarkers Discovery for Colorectal Cancer: A Review on Tumor Endothelial Markers as Perspective Candidates.Disease markers · 2016Review
- RhoC maintains vascular homeostasis by regulating VEGF-induced signaling in endothelial cells.Journal of cell science · 2015Article
- Phosphorylation of Cdc42 effector protein-4 (CEP4) by protein kinase C promotes motility of human breast cells.The Journal of biological chemistry · 2014Article
- Rho GAPs and GEFs: controling switches in endothelial cell adhesion.Cell adhesion & migration · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Persistent cellular migration requires efficient protrusion of the front of the cell, the leading edge where the actin cytoskeleton and cell-substrate adhesions undergo constant rearrangement. Rho family GTPases are essential regulators of the actin cytoskeleton and cell adhesion dynamics. Here, we examined the role of the RhoGEF TEM4, an activator of Rho family GTPases, in regulating cellular migration of endothelial cells. We found that TEM4 promotes the persistence of cellular migration by regulating the architecture of actin stress fibers and cell-substrate adhesions in protruding membranes. Furthermore, we determined that TEM4 regulates cellular migration by signaling to RhoC as suppression of RhoC expression recapitulated the loss-of-TEM4 phenotypes, and RhoC activation was impaired in TEM4-depleted cells. Finally, we showed that TEM4 and RhoC antagonize myosin II-dependent cellular contractility and the suppression of myosin II activity rescued the persistence of cellular migration of TEM4-depleted cells. Our data implicate TEM4 as an essential regulator of the actin cytoskeleton that ensures proper membrane protrusion at the leading edge of migrating cells and efficient cellular migration via suppression of actomyosin contractility.
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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.