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Details on Person The molecular mechanism of Jak activation upon cytokine stim...
| Class:Id | Summation:1112503 |
|---|---|
| _displayName | The molecular mechanism of Jak activation upon cytokine stim... |
| _timestamp | 2025-12-02 15:31:41 |
| created | [InstanceEdit:1112527] Jupe, S, 2010-12-03 |
| literatureReference | [LiteratureReference:1112518] Dual role of the Jak1 FERM and kinase domains in cytokine receptor binding and in stimulation-dependent Jak activation [LiteratureReference:1112592] Distinct domains of the protein tyrosine kinase tyk2 required for binding of interferon-alpha/beta and for signal transduction [LiteratureReference:1112500] Janus kinases in interleukin-2-mediated signaling: JAK1 and JAK3 are differentially regulated by tyrosine phosphorylation [LiteratureReference:1112582] Signaling via IL-2 and IL-4 in JAK3-deficient severe combined immunodeficiency lymphocytes: JAK3-dependent and independent pathways [LiteratureReference:1112529] Prediction of the structure of human Janus kinase 2 (JAK2) comprising the two carboxy-terminal domains reveals a mechanism for autoregulation [LiteratureReference:1112593] Structural requirements of the interleukin-6 signal transducer gp130 for its interaction with Janus kinase 1: the receptor is crucial for kinase activation |
| modified | [InstanceEdit:9975420] Orlic-Milacic, Marija, 2025-12-01 [InstanceEdit:9975763] Orlic-Milacic, Marija, 2025-12-02 |
| text | 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 β receptor subunit is believed to trigger trans-phosphorylation of Jak tyrosines in their kinase activation loop, conferring 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 α/β (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). |
| (summation) | [BlackBoxEvent:1112514] JAK activation [Homo sapiens] |
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