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. © 2014 by the authors; licensee MDPI, Basel, Switzerland.
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CITATION STYLE
Williams, J. J. L., Munro, K. M. A., & Palmer, T. M. (2014). Role of ubiquitylation in controlling suppressor of cytokine signalling 3 (SOCS3) function and expression. Cells. MDPI. https://doi.org/10.3390/cells3020546
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