Next Article in Journal
Systems Analysis of Drug-Induced Receptor Tyrosine Kinase Reprogramming Following Targeted Mono- and Combination Anti-Cancer Therapy
Next Article in Special Issue
The Ufm1 Cascade
Previous Article in Journal
TRPV1: A Potential Drug Target for Treating Various Diseases
Previous Article in Special Issue
HSV-1 ICP0: An E3 Ubiquitin Ligase That Counteracts Host Intrinsic and Innate Immunity
Cells 2014, 3(2), 546-562; doi:10.3390/cells3020546
Review

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

,
 and
*
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)
View Full-Text   |   Download PDF [451 KB, uploaded 30 May 2014]   |   Browse Figures
SciFeed

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).

Share & Cite This Article

Further Mendeley | CiteULike
Export to BibTeX |
EndNote |
RIS
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.

View more citation formats

Related Articles

Article Metrics

Comments

[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert