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Validated All-in-One™ qPCR Primer for RASA1(NM_002890.2) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene is located in the cytoplasm and is part of the GAP1 family of GTPase-activating proteins. The gene product stimulates the GTPase activity of normal RAS p21 but not its oncogenic counterpart. Acting as a suppressor of RAS function, the protein enhances the weak intrinsic GTPase activity of RAS proteins resulting in the inactive GDP-bound form of RAS, thereby allowing control of cellular proliferation and differentiation. Mutations leading to changes in the binding sites of either protein are associated with basal cell carcinomas.
Gene References into function
- We show a novel alternative pathway of apoptosis in human primary cells that is mediated by transcriptionally dependent decreases in p53 and c-Myc and decreases in p21.
- N-terminal fragment generated by caspase cleavage protects cells in a Ras/PI3K/Akt-dependent manner that does not rely on NFkappa B activation
- mutual regulation of Ras and NF1-GAP is essential for normal neuronal differentiation
- p21Ras, hSOS1, and p120GAP are not involved in polycystic ovary disease
- The induction of p21 gene expression is mediated by PPARgamma ligands in lung carcinoma.
- ligation of CD40 on EC increased association of Ras with its effector molecules Raf, Rho, and PI3K. But, it was determined that only PI3K was functional for Ras-induced VEGF transcription.
- executioner caspases control the extent of their own activation by a feedback regulatory mechanism initiated by the partial cleavage of RasGAP that is crucial for cell survival under adverse conditions
- p52Shc couples tyrosine kinase receptors to Ras by recruiting Grb2/Sos complexes.
- an uncleavable N-terminal RasGAP fragment in insulin-secreting cells has a role in increasing resistance toward apoptotic stimuli without affecting glucose-induced insulin secretion
- These results demonstrate that integrin signaling through Arg activates p190 by promoting its association with p120, resulting in recruitment of p190 to the cell periphery where it inhibits Rho.
- novel mutation is decribed, which causes capillary malformation and limb enlargement in a patient from a family with vascular malformations
- the spectrum of clinical manifestations due to mutations in RASA1 is wider than previously thought and also includes typical CMs not associated with AVM/AVF.
- 42 novel RASA1 mutations and the associated phenotype in 44 families.
- RasGAP and Capns1 interaction in oncogenic Ras cells is involved in regulating migration and cell survival.