ArticleCellular signalling2009
Morphological and proliferative abnormalities in renal mesangial cells lacking RhoGDI.
Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- RhoGDI in RBL-2H3 cells acts as a negative regulator of Rho GTPase signaling to inhibit granule exocytosis.Journal of leukocyte biology · 2024Article
- Assessment of roles for the Rho-specific guanine nucleotide dissociation inhibitor Ly-GDI in platelet function: a spatial systems approach.American journal of physiology. Cell physiology · 2017Article
- Small Rho GTPases in the control of cell shape and mobility.Cellular and molecular life sciences : CMLS · 2014Review
- ARHGDIA: a novel gene implicated in nephrotic syndrome.Journal of medical genetics · 2013Article
- Computational analysis of Rho GTPase cycling.PLoS computational biology · 2013Article
- Rho proteins crosstalk via RhoGDIalpha: At random or hierarchically ordered?Communicative & integrative biology · 2012Article
- RhoGDIα-dependent balance between RhoA and RhoC is a key regulator of cancer cell tumorigenesis.Molecular biology of the cell · 2011Article
- The 'invisible hand': regulation of RHO GTPases by RHOGDIs.Nature reviews. Molecular cell biology · 2011Review
- Regulation of Rho GTPase crosstalk, degradation and activity by RhoGDI1.Nature cell biology · 2010Article
- Dynamics of the Rho-family small GTPases in actin regulation and motility.Cell adhesion & migrationReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The regulation of Rho GTPase activities and expression is critical in the development and function of the kidney. Rho GTPase activities and cytosol-membrane cycling are regulated by Rho GDP Dissociation Inhibitor (RhoGDI), and RhoGDI knockout mice develop defects in kidney structure and function that lead to death due to renal failure. It is therefore important to understand the changes in RhoGDI-regulated Rho GTPase activities and cell morphology that lead to kidney failure in RhoGDI (-/-) mice. Here, we characterize a renal mesangial cell line derived from the RhoGDI (-/-) mouse in which we verify the absence of GDI proteins. In the absence of RhoGDI, we show an increase in the specific activity of Rac1, and to a lesser extent, RhoA and Cdc42 GTPases in these cells. This is accompanied by a compensatory decrease in the steady-state protein levels of Rho GTPases. Morphological analysis of RhoGDI (-/-) mesangial cells reveals a decrease in cell spreading and in focal contacts compared to wild-type cells. Finally, RhoGDI (-/-) mesangial cells show a decreased ability to proliferate and survive. These functional and structural changes are likely to contribute to the defects in renal architecture and function observed in the RhoGDI (-/-) mouse.
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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.