ArticleMolecular biology of the cell1998
RhoG GTPase controls a pathway that independently activates Rac1 and Cdc42Hs.
Article in Molecular biology of the cell, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 160 citations in OpenAlex.
- RhoG, Rac1 and Cdc42 cooperation in cell protrusion revealed by multiplexed optogenetics and biosensor imaging.bioRxiv : the preprint server for biology · 2026Article
- The evolution of mammalian Rem2: unraveling the impact of purifying selection and coevolution on protein function, and implications for human disorders.Frontiers in bioinformatics · 2024Article
- Role of RhoG as a regulator of cellular functions: integrating insights on immune cell activation, migration, and functions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- RhoG's Role in T Cell Activation and Function.Frontiers in immunology · 2022Review
- Review
- Role of RhoC in cancer cell migration.Cancer cell international · 2021Review
- Progress in the therapeutic inhibition of Cdc42 signalling.Biochemical Society transactions · 2021Review
- RhoG deficiency abrogates cytotoxicity of human lymphocytes and causes hemophagocytic lymphohistiocytosis.Blood · 2021Article
- Trio family proteins as regulators of cell migration and morphogenesis in development and disease - mechanisms and cellular contexts.Journal of cell science · 2021Review
- Challenge of Bovine Foot Skin Fibroblasts With Digital Dermatitis Treponemes Identifies Distinct Pathogenic Mechanisms.Frontiers in cellular and infection microbiology · 2020Article
- SGEF forms a complex with Scribble and Dlg1 and regulates epithelial junctions and contractility.The Journal of cell biology · 2019Article
- The small GTPase RhoG regulates microtubule-mediated focal adhesion disassembly.Scientific reports · 2019Article
- RHOG Activates RAC1 through CDC42 Leading to Tube Formation in Vascular Endothelial Cells.Cells · 2019Article
- Caveolin-1α regulates primary cilium length by controlling RhoA GTPase activity.Scientific reports · 2019Article
- Congenital Defects in Actin Dynamics of Germinal Center B Cells.Frontiers in immunology · 2019Review
- Human serum albumin and oxidative stress in preeclamptic women and the mechanism of albumin for stress reduction.Heliyon · 2017Article
- Regulation of circular dorsal ruffles, macropinocytosis, and cell migration by RhoG and its exchange factor, Trio.Molecular biology of the cell · 2017Article
- A RhoG-mediated signaling pathway that modulates invadopodia dynamics in breast cancer cells.Journal of cell science · 2017Article
- Apoptotic cell recognition receptors and scavenger receptors.Immunological reviews · 2016Review
- Platelet Rho GTPases-a focus on novel players, roles and relationships.The Biochemical journal · 2015Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RhoG is a member of the Rho family of GTPases that shares 72% and 62% sequence identity with Rac1 and Cdc42Hs, respectively. We have expressed mutant RhoG proteins fused to the green fluorescent protein and analyzed subsequent changes in cell surface morphology and modifications of cytoskeletal structures. In rat and mouse fibroblasts, green fluorescent protein chimera and endogenous RhoG proteins colocalize according to a tubular cytoplasmic pattern, with perinuclear accumulation and local concentration at the plasma membrane. Constitutively active RhoG proteins produce morphological and cytoskeletal changes similar to those elicited by a simultaneous activation of Rac1 and Cdc42Hs, i.e., the formation of ruffles, lamellipodia, filopodia, and partial loss of stress fibers. In addition, RhoG and Cdc42Hs promote the formation of microvilli at the cell apical membrane. RhoG-dependent events are not mediated through a direct interaction with Rac1 and Cdc42Hs targets such as PAK-1, POR1, or WASP proteins but require endogenous Rac1 and Cdc42Hs activities: coexpression of a dominant negative Rac1 impairs membrane ruffling and lamellipodia but not filopodia or microvilli formation. Conversely, coexpression of a dominant negative Cdc42Hs only blocks microvilli and filopodia, but not membrane ruffling and lamellipodia. Microtubule depolymerization upon nocodazole treatment leads to a loss of RhoG protein from the cell periphery associated with a reversal of the RhoG phenotype, whereas PDGF or bradykinin stimulation of nocodazole-treated cells could still promote Rac1- and Cdc42Hs-dependent cytoskeletal reorganization. Therefore, our data demonstrate that RhoG controls a pathway that requires the microtubule network and activates Rac1 and Cdc42Hs independently of their growth factor signaling pathways.
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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.