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http://purl.uniprot.org/citations/11448776http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11448776http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11448776http://www.w3.org/2000/01/rdf-schema#comment"Ca(2+) is a universal second messenger that is critical for cell growth and is intimately associated with many Ras-dependent cellular processes such as proliferation and differentiation. Ras is a small GTP binding protein that operates as a molecular switch regulating the control of gene expression, cell growth, and differentiation through a pathway from receptors to mitogen-activated protein kinases (MAPKs). A role for intracellular Ca(2+) in the activation of Ras has been previously demonstrated, e.g., via the nonreceptor tyrosine kinase PYK2 and by Ca(2+)/calmodulin-dependent guanine nucleotide exchange factors (GEFs) such as Ras-GRF; however, there is no Ca(2+)-dependent mechanism for direct inactivation. An important advance toward greater understanding of the complex coordination within the Ras-signaling network is the spatio-temporal analysis of signaling events in vivo. Here, we describe the identification of CAPRI (Ca(2+)-promoted Ras inactivator), a Ca(2+)-dependent Ras GTPase-activating protein (GAP) that switches off the Ras-MAPK pathway following a stimulus that elevates intracellular Ca(2+). Analysis of the spatio-temporal dynamics of CAPRI indicates that Ca(2+) regulates the GAP by a fast C2 domain-dependent translocation mechanism."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.org/dc/terms/identifier"doi:10.1016/s0960-9822(01)00261-5"xsd:string
http://purl.uniprot.org/citations/11448776http://purl.org/dc/terms/identifier"doi:10.1016/s0960-9822(01)00261-5"xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/author"Cullen P.J."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/author"Cullen P.J."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/author"Kupzig S."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/author"Kupzig S."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/author"Lockyer P.J."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/author"Lockyer P.J."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/name"Curr. Biol."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/name"Curr. Biol."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/pages"981-986"xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/pages"981-986"xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/title"CAPRI regulates Ca(2+)-dependent inactivation of the Ras-MAPK pathway."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/title"CAPRI regulates Ca(2+)-dependent inactivation of the Ras-MAPK pathway."xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/11448776http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/11448776http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11448776
http://purl.uniprot.org/citations/11448776http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11448776
http://purl.uniprot.org/citations/11448776http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11448776
http://purl.uniprot.org/citations/11448776http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11448776