ArticleThe Biochemical journal2001
RhoGDI-binding-defective mutant of Cdc42Hs targets to membranes and activates filopodia formation but does not cycle with the cytosol of mammalian cells.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Molecular mechanism of regulation of RhoA GTPase by phosphorylation of RhoGDI.Biophysical journal · 2024Article
- Trapping of CDC42 C-terminal variants in the Golgi drives pyrin inflammasome hyperactivation.The Journal of experimental medicine · 2022Article
- A Complete Survey of RhoGDI Targets Reveals Novel Interactions with Atypical Small GTPases.Biochemistry · 2021Article
- Article
- A novel disorder involving dyshematopoiesis, inflammation, and HLH due to aberrant CDC42 function.The Journal of experimental medicine · 2019Article
- Establishment of a robust single axis of cell polarity by coupling multiple positive feedback loops.Nature communications · 2013Article
- Flippase-mediated phospholipid asymmetry promotes fast Cdc42 recycling in dynamic maintenance of cell polarity.Nature cell biology · 2012Article
- Identification and characterisation of the RalA-ERp57 interaction: evidence for GDI activity of ERp57.PloS one · 2012Article
- The 'invisible hand': regulation of RHO GTPases by RHOGDIs.Nature reviews. Molecular cell biology · 2011Review
- Dual modes of cdc42 recycling fine-tune polarized morphogenesis.Developmental cell · 2009Article
- The polybasic region of Rac1 modulates bacterial uptake independently of self-association and membrane targeting.The Journal of biological chemistry · 2008Article
- The Parkinson's disease-associated protein, leucine-rich repeat kinase 2 (LRRK2), is an authentic GTPase that stimulates kinase activity.Experimental cell research · 2007Article
- Central roles of small GTPases in the development of cell polarity in yeast and beyond.Microbiology and molecular biology reviews : MMBR · 2007Review
- Use of bimolecular fluorescence complementation to study in vivo interactions between Cdc42p and Rdi1p of Saccharomyces cerevisiae.Eukaryotic cell · 2007Article
- Beta8 integrin binds Rho GDP dissociation inhibitor-1 and activates Rac1 to inhibit mesangial cell myofibroblast differentiation.The Journal of biological chemistry · 2006Article
- Yersinia pseudotuberculosis spatially controls activation and misregulation of host cell Rac1.PLoS pathogens · 2005Article
- RhoGDI: multiple functions in the regulation of Rho family GTPase activities.The Biochemical journal · 2005Review
- Regulation of membrane trafficking by a novel Cdc42-related protein in Caenorhabditis elegans epithelial cells.Molecular biology of the cell · 2005Article
- An activating mutant of Rac1 that fails to interact with Rho GDP-dissociation inhibitor stimulates membrane ruffling in mammalian cells.The Biochemical journal · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have identified a mutant of the human G-protein Cdc42Hs, R66E, that fails to form a detectable complex with the GDP-dissociation inhibitor RhoGDI in cell-free systems or in intact cells. This point mutant is prenylated, binds guanine nucleotide and interacts with GTPase-activating protein in a manner indistinguishable from wild-type Cdc42Hs. Immunofluorescence localization studies revealed that this RhoGDI-binding-defective mutant is found predominantly in the Golgi apparatus, with a staining pattern similar to that of the wild-type protein. However, unlike wild-type Cdc42Hs, which is distributed in both the microsomal membrane and cytosolic fractions, studies using differential centrifugation show that prenylated R66E Cdc42Hs is found exclusively in association with lipid bilayers. Additionally, whereas the overexpression of RhoGDI results in an apparent translocation of wild-type Cdc42Hs from the Golgi apparatus into the cytosol, identical RhoGDI-overexpression conditions do not alter the Golgi localization of the R66E mutant. Furthermore, overexpression of this RhoGDI-binding-defective mutant of Cdc42Hs seems to activate redistribution of the actin cytoskeleton and filopodia formation in fibroblasts in a manner indistinguishable from the wild-type protein. Taken together, these results suggest that the interaction of Cdc42Hs with RhoGDI is not essential for proper membrane targeting of nascent prenylated Cdc42Hs in mammalian cells; neither is this interaction an essential part of the mechanism by which Cdc42Hs activates filopodia formation. However, it does seem that redistribution of Cdc42Hs to the cytosolic compartment is absolutely dependent on RhoGDI interaction.
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.