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Cells 2014, 3(2), 546-562; doi:10.3390/cells3020546

Role of Ubiquitylation in Controlling Suppressor of Cytokine Signalling 3 (SOCS3) Function and Expression

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8QQ, UK
* Author to whom correspondence should be addressed.
Received: 30 December 2013 / Revised: 1 May 2014 / Accepted: 4 May 2014 / Published: 30 May 2014
(This article belongs to the Special Issue Protein Ubiquitination)
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The realisation that unregulated activation of the Janus kinase–signal transducer and activator of transcription (JAK–STAT) pathway is a key driver of a wide range of diseases has identified its components as targets for therapeutic intervention by small molecule inhibitors and biologicals. In this review, we discuss JAK-STAT signalling pathway inhibition by the inducible inhibitor “suppressor of cytokine signaling 3 (SOCS3), its role in diseases such as myeloproliferative disorders, and its function as part of a multi-subunit E3 ubiquitin ligase complex. In addition, we highlight potential applications of these insights into SOCS3-based therapeutic strategies for management of conditions such as vascular re-stenosis associated with acute vascular injury, where there is strong evidence that multiple processes involved in disease progression could be attenuated by localized potentiation of SOCS3 expression levels.
Keywords: SOCS3; JAK; STAT; inflammation; ubiquitin; proteasomal degradation SOCS3; JAK; STAT; inflammation; ubiquitin; proteasomal degradation
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Williams, J.J.L.; Munro, K.M.A.; Palmer, T.M. Role of Ubiquitylation in Controlling Suppressor of Cytokine Signalling 3 (SOCS3) Function and Expression. Cells 2014, 3, 546-562.

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