Human Interaction Network Ontology

Last uploaded: June 27, 2014
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Id http://purl.obolibrary.org/obo/HINO_0006480
http://purl.obolibrary.org/obo/HINO_0006480
Preferred Name

JAK activation
Definitions
Authored: Ray, K, 2010-12-13 has a Stoichiometric coefficient of 12 Edited: Jupe, S, 2010-12-10 The molecular mechanism of Jak activation upon cytokine stimulation is not understood in detail (Haan et al. 2008). Cytokine-induced receptor aggregation and the resulting close proximity of Jaks bound to the beta receptor subunit is believed to trigger trans-phosphorylation of Jak tyrosines in their kinase activation loop, confering kinase activity. This active state is believed to be maintained by further autocatalytic tyrosine phosphorylations. For JAK1 the activation loop tyrosine residues are predicted by homology with models of JAK2 (Lindauer et al. 2001) to be Tyr-1034/1035. Mutation of Tyr-1034 abolishes JAK1 kinase activity (Liu et al. 1997). Evidence supporting JAK1 transphosphorylation includes JAK1 mutant cell lines, which cannot activate Tyk2 after stimulation with interferon alpha/beta (Velazquez et al. 1995) and the observation that IL-2 cannot activate JAK1 in the absence of JAK3 (Oakes et al. 1996). The receptor is not merely a docking site for JAKs as certain gp130 residues are required for JAK1 activation, but not essential for JAK1 binding (Haan et al. 2002). Reviewed: Rose-John, S, 2011-02-11
Type http://www.w3.org/2002/07/owl#Class

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JAK activation
comment
Authored: Ray, K, 2010-12-13
has a Stoichiometric coefficient of 12
Edited: Jupe, S, 2010-12-10
The molecular mechanism of Jak activation upon cytokine stimulation is not understood in detail (Haan et al. 2008). Cytokine-induced receptor aggregation and the resulting close proximity of Jaks bound to the beta receptor subunit is believed to trigger trans-phosphorylation of Jak tyrosines in their kinase activation loop, confering kinase activity. This active state is believed to be maintained by further autocatalytic tyrosine phosphorylations. For JAK1 the activation loop tyrosine residues are predicted by homology with models of JAK2 (Lindauer et al. 2001) to be Tyr-1034/1035. Mutation of Tyr-1034 abolishes JAK1 kinase activity (Liu et al. 1997). Evidence supporting JAK1 transphosphorylation includes JAK1 mutant cell lines, which cannot activate Tyk2 after stimulation with interferon alpha/beta (Velazquez et al. 1995) and the observation that IL-2 cannot activate JAK1 in the absence of JAK3 (Oakes et al. 1996). The receptor is not merely a docking site for JAKs as certain gp130 residues are required for JAK1 activation, but not essential for JAK1 binding (Haan et al. 2002).
Reviewed: Rose-John, S, 2011-02-11
prefLabel
JAK activation
definition source
Pubmed8134389
Reactome, http://www.reactome.org
Pubmed9382798
Pubmed8986719
Pubmed11287676
Pubmed11742534
Pubmed7531704
Pubmed18178840
Pubmed8272873
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HINO:0006480
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Reactome Database ID Release 431112514
ReactomeREACT_27288
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