Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity.
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping.
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara.
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods.
Purification, characterization, and western blot analysis of human GTPase-activating protein from native and recombinant sources.
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GAP stimulates GTPase activity of normal but not oncogenic Ras p21
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Two forms of GAP (120 kDa and 95 kDa) purified from human placenta
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Both forms have similar biological specific activities
Regulation of the Ras signaling pathway by GTPase-activating protein in PC12 cells.
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GAP acts as negative regulator rather than effector of Ras signaling
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Overexpression of membrane-targeted GAP inhibits NGF-induced differentiation
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GAP inhibition is bypassed by oncogenic Ras or Raf
Purification, characterization, and cellular localization of the 100-kDa human placental GTPase-activating protein.
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GAP localized to cytoplasm of trophoblasts in human placenta
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p100-GAP is placenta-specific isoform
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GAP present at approximately 0.1% of total protein in placenta
The N-terminal region of GAP regulates cytoskeletal structure and cell adhesion.
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GAP-N (SH2-SH3 region) binds constitutively to p190RhoGAP
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GAP-N expression disrupts actin stress fibers and focal contacts
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GAP-N impairs cell adhesion to fibronectin
The Ras-RasGAP complex structural basis for GTPase activation and its loss in oncogenic Ras mutants.
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Crystal structure of Ras-GAP complex at 2.5 angstrom resolution
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Arginine-789 of GAP stabilizes transition state in active site
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Explains how Gly12 and Gln61 mutations activate Ras oncogenic potential
EphB4 promotes or suppresses Ras/MEK/ERK pathway in a context-dependent manner: Implications for EphB4 as a cancer target.
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p120 RasGAP mediates EphB4-induced suppression of ERK in endothelial cells
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Knockdown of RasGAP attenuates EphB4 inhibitory effect on ERK
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Context-dependent effects depend on coupling to different effectors
Mutations in Chromatin Modifier and Ephrin Signaling Genes in Vein of Galen Malformation.
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RASA1-EPHB4 pathway mutations cause vein of Galen malformations
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VOGM-associated EphB4 mutations decrease binding to RASA1
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Incomplete penetrance suggests two-hit mechanism
Partial cleavage of RasGAP by caspases is required for cell survival in mild stress conditions.
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Caspase-3 cleavage of RasGAP generates anti-apoptotic fragment N
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Fragment N activates Akt to prevent caspase amplification
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Uncleavable RasGAP mutant cells undergo apoptosis under mild stress
Modulation of guanine nucleotides bound to Ras in NIH3T3 cells by oncogenes, growth factors, and the GTPase activating protein (GAP).
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GAP overexpression reduces basal Ras-GTP levels in cells
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PDGF and v-Src increase Ras-GTP through tyrosine kinase activation
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Demonstrates GAP function in intact mammalian cells
A novel RASA1 mutation causing capillary malformation-arteriovenous malformation (CM-AVM) presenting during pregnancy.
GAP domains responsible for ras p21-dependent inhibition of muscarinic atrial K+ channel currents.
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SH2-SH3 domains of GAP responsible for K+ channel inhibition
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Ras p21 binding induces conformational change allowing SH2-SH3 function
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Demonstrates effector-like function of GAP N-terminal region
Ras-GTPase activating protein (GAP) a putative effector for Ras.
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GAP may function as Ras effector through N-terminal domain
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G3BP identified as GAP-SH3 binding protein
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GAP N-terminal region triggers downstream signals
Tarp regulates early Chlamydia-induced host cell survival through interactions with the human adaptor protein SHC1.
Identification of amino acid residues of Ras protein that are essential for signal-transducing activity but not for enhancement of GTPase activity by GAP.
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Ras effector region residues Val45 and Gly48 essential for signal transduction
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These residues not required for GAP-mediated GTPase enhancement
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Distinguishes effector function from GAP regulation
Phosphorylation sites in the PDGF receptor with different specificities for binding GAP and PI3 kinase in vivo.
GTPase-activating protein and phosphatidylinositol 3-kinase bind to distinct regions of the platelet-derived growth factor receptor beta subunit.
Tyrosine phosphorylation of caveolin-2 at residue 27: differences in the spatial and temporal behavior of phospho-Cav-2 (pY19 and pY27).
A novel role for Gab1 and SHP2 in epidermal growth factor-induced Ras activation.
A quantitative protein interaction network for the ErbB receptors using protein microarrays.
Capns1, a new binding partner of RasGAP-SH3 domain in K-Ras(V12) oncogenic cells: modulation of cell survival and migration.
p120Ras-GAP binds the DLC1 Rho-GAP tumor suppressor protein and inhibits its RhoA GTPase and growth-suppressing activities.
Abi1/Hssh3bp1 pY213 links Abl kinase signaling to p85 regulatory subunit of PI-3 kinase in regulation of macropinocytosis in LNCaP cells.
Tyrosine-phosphorylated caveolin-1 blocks bacterial uptake by inducing Vav2-RhoA-mediated cytoskeletal rearrangements.
Adaptor protein Nck1 interacts with p120 Ras GTPase-activating protein and regulates its activity.
Charting the molecular links between driver and susceptibility genes in colorectal cancer.
Enhanced prediction of Src homology 2 (SH2) domain binding potentials using a fluorescence polarization-derived c-Met, c-Kit, ErbB, and androgen receptor interactome.
ABL2 suppresses FLT3-ITD-induced cell proliferation through negative regulation of AKT signaling.
A reference map of the human binary protein interactome
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
In vivo binding properties of SH2 domains from GTPase-activating protein and phosphatidylinositol 3-kinase.
Phosphotyrosine-independent binding of a 62-kDa protein to the src homology 2 (SH2) domain of p56lck and its regulation by phosphorylation of Ser-59 in the lck unique N-terminal region.
Overexpression of FAK promotes Ras activity through the formation of a FAK/p120RasGAP complex in malignant astrocytoma cells.
Molecular cloning of cDNAs encoding the GAP-associated protein p190: implications for a signaling pathway from ras to the nucleus.
Binding of GAP to activated PDGF receptors
The tyrosine phosphorylated carboxyterminus of the EGF receptor is a binding site for GAP and PLC-gamma.
Phosphorylation of GAP and GAP-associated proteins by transforming and mitogenic tyrosine kinases.
A Ras-GTPase-activating protein SH3-domain-binding protein.
A cytoplasmic protein stimulates normal N-ras p21 GTPase, but does not affect oncogenic mutants.
Ephrin receptor signaling pathway
RASA1 stimulates RAS GTPase activity
GAP binding to PDGF-beta receptors
Ras:GTP binding to p120-RasGAP
p120-RasGAP activating GTP hydrolysis on RAS
Sphingosine kinase pathway
RAS GAPs stimulating RAS GTPase activity
Deep research on RASA1 gene function and regulation
Cyberian deep research on RASA1 function