ArticleThe Journal of cell biology2017
Receptor tyrosine kinase activation of RhoA is mediated by AKT phosphorylation of DLC1.
Article in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Chromatin accessibility regulates age-dependent nuclear mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Filamin a binds deleted in liver cancer 1 (DLC1) to promote its tumor suppressor activity and inhibit the SRF coactivator MRTF-A.Neoplasia (New York, N.Y.) · 2026Article
- The circDUSP1/miR-429/DLC1 regulatory network affects proliferation, migration, and invasion of triple-negative breast cancer cells.Scientific reports · 2025Article
- Rho-GTPases subfamily: cellular defectors orchestrating viral infection.Cellular & molecular biology letters · 2025Review
- CD73 controls Myosin II-driven invasion, metastasis, and immunosuppression in amoeboid pancreatic cancer cells.Science advances · 2023Article
- The oncogenic miR-429 promotes triple-negative breast cancer progression by degrading DLC1.Aging · 2023Article
- Chylomicrons Regulate Lacteal Permeability and Intestinal Lipid Absorption.Circulation research · 2023Article
- Electric field promotes dermal fibroblast transdifferentiation through activation of RhoA/ROCK1 pathway.International journal of medical sciences · 2023Article
- Article
- Direct interaction of TrkA/CD44v3 is essential for NGF-promoted aggressiveness of breast cancer cells.Journal of experimental & clinical cancer research : CR · 2022Article
- Proteasomal turnover of the RhoGAP tumor suppressor DLC1 is regulated by HECTD1 and USP7.Scientific reports · 2022Article
- Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein.Nature communications · 2021Article
- proBDNF expression induces apoptosis and inhibits synaptic regeneration by regulating the RhoA-JNK pathway in an in vitro post-stroke depression model.Translational psychiatry · 2021Article
- The tumor suppressor activity of DLC1 requires the interaction of its START domain with Phosphatidylserine, PLCD1, and Caveolin-1.Molecular cancer · 2021Article
- The Crossroads between RAS and RHO Signaling Pathways in Cellular Transformation, Motility and Contraction.Genes · 2021Review
- Structural basis for p50RhoGAP BCH domain-mediated regulation of Rho inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- PKCε regulates Rho GTPases and actin cytoskeleton reorganization in non-small cell lung cancer cells.Small GTPases · 2021Article
- Cancer-Associated Point Mutations in theCancer research · 2020Article
- ARHGAP24 inhibits cell proliferation and cell cycle progression and induces apoptosis of lung cancer via a STAT6-WWP2-p27 axis.Carcinogenesis · 2020Article
- Nuclear DLC1 exerts oncogenic function through association with FOXK1 for cooperative activation of MMP9 expression in melanoma.Oncogene · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
We report several receptor tyrosine kinase (RTK) ligands increase RhoA-guanosine triphosphate (GTP) in untransformed and transformed cell lines and determine this phenomenon depends on the RTKs activating the AKT serine/threonine kinase. The increased RhoA-GTP results from AKT phosphorylating three serines (S298, S329, and S567) in the DLC1 tumor suppressor, a Rho GTPase-activating protein (RhoGAP) associated with focal adhesions. Phosphorylation of the serines, located N-terminal to the DLC1 RhoGAP domain, induces strong binding of that N-terminal region to the RhoGAP domain, converting DLC1 from an open, active dimer to a closed, inactive monomer. That binding, which interferes with the interaction of RhoA-GTP with the RhoGAP domain, reduces the hydrolysis of RhoA-GTP, the binding of other DLC1 ligands, and the colocalization of DLC1 with focal adhesions and attenuates tumor suppressor activity. DLC1 is a critical AKT target in DLC1-positive cancer because AKT inhibition has potent antitumor activity in the DLC1-positive transgenic cancer model and in a DLC1-positive cancer cell line but not in an isogenic DLC1-negative cell line.
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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.