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Details on Person A series of sequential phosphorylation events lead to full o...

Class:IdSummation:446704
_displayNameA series of sequential phosphorylation events lead to full o...
_timestamp2010-05-17 16:53:58
created[InstanceEdit:446679] Jupe, S, 2009-11-16
literatureReference[LiteratureReference:165896] Sequential autophosphorylation steps in the interleukin-1 Receptor-associated Kinase-1 Regulate its Availability as an Adapter in Interleukin-1 Signaling
[LiteratureReference:450158] Lys63-linked polyubiquitination of IRAK-1 is required for interleukin-1 receptor- and toll-like receptor-mediated NF-kappaB activation
[LiteratureReference:450177] Effects of IL-1 receptor-associated kinase (IRAK) expression on IL-1 signaling are independent of its kinase activity
[LiteratureReference:446867] Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4
[LiteratureReference:450176] IRAK-4 kinase activity is required for interleukin-1 (IL-1) receptor- and toll-like receptor 7-mediated signaling and gene expression
modified[InstanceEdit:446708] Jupe, S, 2009-11-16
[InstanceEdit:450128] Jupe, S, 2009-12-14
[InstanceEdit:450149] Jupe, S, 2009-12-16
[InstanceEdit:561123] Jupe, S, 2010-03-25
[InstanceEdit:744681] Jupe, S, 2010-05-17
textA series of sequential phosphorylation events lead to full or hyper-phopshorylation of IRAK1. Under in vitro conditions these are all autophosphorylation events. First, Thr-209 is phosphorylated resulting in a conformational change of the kinase domain. Next, Thr-387 in the activation loop is phosphorylated, leading to full enzymatic activity. Several additional residues are phosphorylated in the proline-, serine-, and threonine-rich (ProST) region between the N-terminal death domain and kinase domain. Hyperphosphorylation of this region leads to dissociation of IRAK1 from the upstream adapters MyD88 and Tollip. The significance of these phosphorylation events is not clear; the kinase activity of IRAK1 is dispensable for IL1-induced NFkB and MAP kinase activation (Knop & Martin, 1999), unlike that of IRAK4 (Suzuki et al. 2002; Kozicak-Holbro et al. 2007), so IRAK1 is believed to act primarily as an adaptor for TRAF6 (Conze et al. 2008).
(summation)[Reaction:446701] IRAK4-activated IRAK1 autophosphorylates [Homo sapiens]
[Reaction:975125] Multiple IRAK1 autophosphorylation steps within the complex pIRAK4:MyD88:activated TLR7/8 or 9 [Homo sapiens]
[Reaction:975853] Multiple IRAK1 autophosphorylation within the complex p-IRAK4:oligo MyD88:activated TLR [Homo sapiens]
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