ArticleMolecular and cellular biology2006
Characterization of R-ras3/m-ras null mice reveals a potential role in trophic factor signaling.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Revisiting RAS family GTPase signaling: effector selectivity and oncogenic bypass.The Biochemical journal · 2026Review
- Structure of SHOC2-KRAS-PP1C complex reveals RAS isoform-specific determinants and insights into targeting complex assembly by RAS inhibitors.Nature communications · 2026Article
- Structural insights into the role of SHOC2-MRAS-PP1C complex in RAF activation.The FEBS journal · 2023Review
- Structure of the SHOC2-MRAS-PP1C complex provides insights into RAF activation and Noonan syndrome.Nature structural & molecular biology · 2022Article
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- The RASopathies: from pathogenetics to therapeutics.Disease models & mechanisms · 2022Review
- MRAS: A Close but Understudied Member of the RAS Family.Cold Spring Harbor perspectives in medicine · 2018Review
- Absence of M-Ras modulates social behavior in mice.BMC neuroscience · 2015Article
- Genetic dissection of plexin signaling in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The Ras-like protein R-Ras2/TC21 is important for proper mammary gland development.Molecular biology of the cell · 2012Article
- Article
- Genome-wide association studies in atherosclerosis.Current atherosclerosis reports · 2011Review
- Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology.EMBO reports · 2009Article
- The M-Ras-RA-GEF-2-Rap1 pathway mediates tumor necrosis factor-alpha dependent regulation of integrin activation in splenocytes.Molecular biology of the cell · 2007Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
R-Ras3/M-Ras is a member of the RAS superfamily of small-molecular-weight GTP-binding proteins. Previous studies have demonstrated high levels of expression in several regions of the central nervous system, and a constitutively active form of M-Ras promotes cytoskeletal reorganization, cellular transformation, survival, and differentiation. However, the physiological functions of M-Ras during embryogenesis and postnatal development have not been elucidated. By using a specific M-Ras antibody, we demonstrated a high level of M-Ras expression in astrocytes, in addition to neurons. Endogenous M-Ras was activated by several trophic factors in astrocytes, including epidermal growth factor (EGF), basic fibroblast growth factor, and hepatocyte growth factor. Interestingly, M-Ras activation by EGF was more sustained compared to prototypic Ras. A mouse strain deficient in M-Ras was generated to investigate its role in development. M-Ras null mice appeared phenotypically normal, and there was a lack of detectable morphological and neurological defects. In addition, primary astrocytes derived from Mras(-/-) mice did not appear to display substantial alterations in the activation of both the mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways in response to trophic factors.
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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.