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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
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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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Abstract

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 3.0).

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MDPI and ACS Style

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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