Query author contributions in Reactome

Reactome depends on collaboration between our curation team and outside experts to assemble and peer-review its pathway modules. The integration of ORCID within Reactome enables us to meet a key challenge with authoring, curating and reviewing biological information by incentivizing and crediting the external experts that contribute their expertise and time to the Reactome curation process. More information is available at ORCID and Reactome.

If you have an ORCID ID that is not listed on this page, please forward this information to us and we will update your Reactome pathway records.

Details on Person Mechanistic models of receptor activation, largely based on ...

Class:Id	Summation:8983749
_displayName	Mechanistic models of receptor activation, largely based on ...
_timestamp	2017-05-10 10:20:48
created	[InstanceEdit:8983731] Jupe, Steve, 2017-03-27
literatureReference	[LiteratureReference:1213501] Activation of the interleukin 2 receptor: a possible role for tyrosine phosphatases [LiteratureReference:1112544] Principles of interleukin (IL)-6-type cytokine signalling and its regulation [LiteratureReference:8983737] Prerequisites for Functional Interleukin 31 Signaling and Its Feedback Regulation by Suppressor of Cytokine Signaling 3 (SOCS3) [LiteratureReference:8983739] Novel role of Janus kinase 1 in the regulation of oncostatin M receptor surface expression [LiteratureReference:8983735] The Jak1 SH2 domain does not fulfill a classical SH2 function in Jak/STAT signaling but plays a structural role for receptor interaction and up-regulation of receptor surface expression [LiteratureReference:8983740] Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protein Shc is specifically recruited to rhe oncostatin M receptor [LiteratureReference:448635] Characterization of the signaling capacities of the novel gp130-like cytokine receptor [LiteratureReference:9005653] Oncostatin M and interleukin-31: Cytokines, receptors, signal transduction and physiology [LiteratureReference:9005781] Box 2 region of the oncostatin M receptor determines specificity for recruitment of Janus kinases and STAT5 activation
modified	[InstanceEdit:9005644] Jupe, Steve, 2017-05-09 [InstanceEdit:9005780] Jupe, Steve, 2017-05-10
text	Mechanistic models of receptor activation, largely based on experimental data obtained with the interleukin-2 and -6 receptors, suggest that assembly of interleukin receptor complexes and the consequent proximity of JAK tyrosine-protein kinases bound to so-called box motifs in the cytoplasmic region of the receptor subunits are the trigger for activating JAK phosphorylation and consequent receptor activation (Ellery et al. 2000, Heinrich et al. 2003). Interleukin-31 receptor subunit alpha (IL31RA) can bind and signal through Tyrosine-protein kinase JAK1 (JAK1), which is strongly tyrosine-phosphorylated upon receptor activation (Dreuw et al. 2004), leading to tyrosine-phosphorylation and activation of Signal transducer and activator of transcription 3 (STAT3), STAT5 and marginally, STAT1. Introduction of a stop codon that prevents expression of a functional box motif within IL31RA resulted in a complete loss of Interleukin-31 (IL31)-induced STAT3 activation. Similar effects were observed when highly conserved amino acids within the box motif were mutated (Maier et al. 2015), indicating that IL31RA JAK binding is essential for STAT activation. Oncostatin-M-specific receptor subunit beta (OSMR) surface expression is enhanced by JAK1 binding (Radtke et al. 2002, 2005).
(summation)	[BlackBoxEvent:8983746] JAK1 in IL31:IL31RA:JAK1:OSMR:JAK1 is phosphorylated [Homo sapiens]
[Change default viewing format]

No pathways have been reviewed or authored by Mechanistic models of receptor activation, largely based on ... (8983749)