About: Ras-Independent Cell-Mediated Cytotoxicity Pathway

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Attributes	Values
rdf:type	Class
rdfs:label	Ras-Independent Cell-Mediated Cytotoxicity Pathway
rdfs:subClassOf	Immune Response Regulation Pathway
Semantic_Type	Functional Concept
Preferred_Name	Ras-Independent Cell-Mediated Cytotoxicity Pathway
UMLS_CUI	C1514726
BioCarta_ID	h_nkcellsPathway
ALT_DEFINITION	NK (natural killer) cells are lymphocytes distinct from B and T cells that induce perforin-mediated lysis of tumor cells and virus-infected cells. NK cell-mediated cytotoxicity is activated by glycoproteins on the cell surface (activating receptors) and inhibited by MHC-1 with self-peptide bound. The MHC-1 inhibitory signal through Ig-family or lectin receptors prevents NK cells from killing normal cells. Abnormal MHC-1 expression in infected or tumor cells results in the release of perforin, the lysis of the abnormal cell and the release of cytokines that stimulate the immune response. MAP kinase inhibitors, but not ras inhibitors, are able to block NK cell cytotoxicity, indicating that the pathway can function by a ras-independent manner that involves the MAP kinase pathway. This pathway includes phosphoinositide-3-kinase (PI3K) as a key component, followed by Rac1 and the exchange factor Vav. The tyrosine kinase SYK and LAT may provide an additional pathway for activation of MAP kinases leading to NK cell activation, and also Pyk-2 activation by integrins. The protein tyrosine phosphatase SHP-1 appears to mediate the cytotoxicity inhibitory signal that blocks lysis of normal cells. The balance of these positive and negative signaling pathways regulates the role of NK cells in the immune response.BIOCARTA
Legacy_Concept_Name	Ras-Independent_Cell-Mediated_Cytotoxicity_Pathway
FULL_SYN	Ras-Independent pathway in NK cell-mediated cytotoxicityPTBIOCARTA Ras-Independent Cell-Mediated Cytotoxicity PathwayPTNCI
code	C39165
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