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- NCIT_C39241 NCIT_NHC0 "C39241" @default.
- NCIT_C39241 NCIT_P106 "Functional Concept" @default.
- NCIT_C39241 NCIT_P108 "TNF Stress Related Signaling Pathway" @default.
- NCIT_C39241 NCIT_P207 "C1515167" @default.
- NCIT_C39241 NCIT_P216 "h_stressPathway" @default.
- NCIT_C39241 NCIT_P325 "TNF acts on several different signaling pathways through two cell surface receptors, TNFR1 and TNFR2 to regulate apoptotic pathways, NF-kB activation of inflammation, and activate stress-activated protein kinases (SAPKs). Interaction of TNFR1 with TRADD leads to activation of NF-kB and apoptosis pathways, while interaction with TRAF2 has generally been thought to be involved in stress kinase and NF-kB activation but is not required for TNF to induce apoptosis. Activation of NF-kB is mediated by TRAF2 through the NIK kinase and also by RIP but the observation that TNF activates NF-kB in mice lacking TRAF2 indicates that TRAF-2 does not play an essential role in this process. Stress-activated protein kinases, also called JNKs, are a family of map kinases activated by cellular stress and inflammatory signals. Binding of TNF to the TNFR1 receptor activates the germinal center kinase (GCK) through the TNF adaptor Traf2, activating the map kinase MEKK1. Both GCK and MEKK1 interact with Traf2, and GCK is required for MEKK1 activation by TNF, but GCK kinase activity does not appear to be required for MEKK1 activation. Instead, GCK activates MEKK1 by causing MEKK1 oligomerization and autophosphorylation. Tank increases the affinity of Traf2 for GCK to increase Map kinase activation by TNF. Once activated, MEKK1 stands at the top of a map kinase pathway leading to transcriptional regulation, including JNK phosphorylation of c-Jun to stimulate transcriptional activation by AP-1, a heterodimer of c-jun and fos or ATF proteins. The activation of the p38 Map kinase also contributes to AP-1 activation leading to the transcriptional activation of many stress and growth related genes. RIP has been suggested as a component of the p38 pathway in addition to playing a role in NF-kB activation. MEKK1 knockout mice support the role of MEKK1 in JNK activation in some cells but did not support MEKK1 dependent activation of NF-kB. Alternative redundant mechanisms may obscure the role of MEKK1 in NF-kB mechanisms. TNF activation of stress kinase pathways and downstream transcription factors may help to modulate the apoptotic pathways also activated by TNF. (This definition may be outdated - see the DesignNote.)" @default.
- NCIT_C39241 NCIT_P366 "TNF_Stress_Related_Signaling_Pathway" @default.
- NCIT_C39241 NCIT_P98 "The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA Definition might be outdated or inaccurate. Please see the Terms and Conditions for Use at http://www.biocarta.com/." @default.
- NCIT_C39241 normalizedInformationContent "79.853901415798049" @default.
- NCIT_C39241 referenceCount "21" @default.
- NCIT_C39241 hasExactSynonym "TNF Stress Related Signaling Pathway" @default.
- NCIT_C39241 hasExactSynonym "TNF/Stress Related Signaling" @default.
- NCIT_C39241 type Class @default.
- NCIT_C39241 isDefinedBy ncit.owl @default.
- NCIT_C39241 label "TNF Stress Related Signaling Pathway" @default.
- NCIT_C39241 subClassOf NCIT_C17132 @default.
- NCIT_C39241 subClassOf NCIT_C20633 @default.
- NCIT_C39241 subClassOf NCIT_C39241 @default.