ArticleMolecular and cellular biology1997
Aberrant Ras regulation and reduced p190 tyrosine phosphorylation in cells lacking p120-Gap.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 78 citations in OpenAlex.
- Clinically observed RASA1 missense mutants exhibit diverse RasGAP protein behaviors in vitro.The Journal of biological chemistry · 2026Article
- Clinically observedbioRxiv : the preprint server for biology · 2025Article
- p120 RasGAP and ZO-2 are essential for Hippo signaling and tumor-suppressor function mediated by p190A RhoGAP.Cell reports · 2023Article
- Crosstalk of the Caspase Family and Mammalian Target of Rapamycin Signaling.International journal of molecular sciences · 2021Review
- The GTPase-activating protein p120RasGAP has an evolutionarily conserved "FLVR-unique" SH2 domain.The Journal of biological chemistry · 2020Article
- The NF2 tumor suppressor merlin interacts with Ras and RasGAP, which may modulate Ras signaling.Oncogene · 2019Article
- Crystal structures of p120RasGAP N-terminal SH2 domain in its apo form and in complex with a p190RhoGAP phosphotyrosine peptide.PloS one · 2019Article
- p120RasGAP Protein Mediates Netrin-1 Protein-induced Cortical Axon Outgrowth and Guidance.The Journal of biological chemistry · 2016Article
- RasGAP Promotes Autophagy and Thereby Suppresses Platelet-Derived Growth Factor Receptor-Mediated Signaling Events, Cellular Responses, and Pathology.Molecular and cellular biology · 2015Article
- p120RasGAP is a mediator of rho pathway activation and tumorigenicity in the DLD1 colorectal cancer cell line.PloS one · 2014Article
- Nonredundant functions for Ras GTPase-activating proteins in tissue homeostasis.Science signaling · 2013Review
- RASA1 maintains the lymphatic vasculature in a quiescent functional state in mice.The Journal of clinical investigation · 2012Article
- Differential Regulation of RasGAPs in Cancer.Genes & cancer · 2011Article
- A FAK-p120RasGAP-p190RhoGAP complex regulates polarity in migrating cells.Journal of cell science · 2009Article
- Overexpression of E-cadherin on melanoma cells inhibits chemokine-promoted invasion involving p190RhoGAP/p120ctn-dependent inactivation of RhoA.The Journal of biological chemistry · 2009Article
- Annexin A6 inhibits Ras signalling in breast cancer cells.Oncogene · 2009Article
- Impaired Akt activity down-modulation, caspase-3 activation, and apoptosis in cells expressing a caspase-resistant mutant of RasGAP at position 157.Molecular biology of the cell · 2005Article
- Partial cleavage of RasGAP by caspases is required for cell survival in mild stress conditions.Molecular and cellular biology · 2004Article
- v-Src induces Shc binding to tyrosine 63 in the cytoplasmic domain of the LDL receptor-related protein 1.Oncogene · 2003Article
- Deregulation of the Egfr/Ras signaling pathway induces age-related brain degeneration in the Drosophila mutant vap.Molecular biology of the cell · 2003Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ras guanine nucleotide-binding protein functions as a molecular switch in signalling downstream of protein-tyrosine kinases. Ras is activated by exchange of GDP for GTP and is turned off by hydrolysis of bound GTP to GDP. Ras itself has a low intrinsic GTPase activity that can be stimulated by GTPase-activating proteins (GAPs), including p120-Gap and neurofibromin. These GAPs possess a common catalytic domain but contain distinct regulatory elements that may couple different external signals to control of the Ras pathway. p120-Gap, for example, has two N-terminal SH2 domains that directly recognize phosphotyrosine motifs on activated growth factor receptors and cytoplasmic phosphoproteins. To analyze the role of p120-Gap in Ras regulation in vivo, we have used fibroblasts derived from mouse embryos with a null mutation in the gene for p120-Gap (Gap). Platelet-derived growth factor stimulation of Gap-/- cells led to an abnormally large increase in the level of Ras-GTP and in the duration of mitogen-activated protein (MAP) kinase activation compared with wild-type cells, suggesting that p120-Gap is specifically activated following growth factor stimulation. Induction of DNA synthesis in response to platelet-derived growth factor and morphological transformation by the v-src and EJ-ras oncogenes were not significantly affected by the absence of p120-Gap. However, we found that normal tyrosine phosphorylation of p190-rhoGap, a cytoplasmic protein that associates with the p120-Gap SH2 domains, was dependent on the presence of p120-Gap. Our results suggest that p120-Gap has specific functions in downregulating the Ras/MAP kinase pathway following growth factor stimulation, and in modulating the phosphorylation of p190-rhoGap, but is not required for mitogenic signalling.
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