By G. Da Silva Xavier
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Extra resources for Advances in Protein Kinases
2007), selective inhibition of IL-6 trans-signaling using sgp130Fc or related therapeutics might prove a useful approach to arrest the development of colon cancer and other tumours in which a pathophysiological role for IL-6 trans-signaling could be identified. 6. Conclusions Progress in our understanding of the molecular basis of cytokine signaling and the subsequent identification of the importance of JAK mutations and hyperactivation of STAT3 in disease states has improved our understanding of the pathogenesis of RA, PV and several cancers.
2001) SOCS proteins: negative regulators of cytokine signaling, Stem Cells. 19: 378-387. A. A. (2001) Interferon-kappa, a novel type I interferon expressed in human keratinocytes, J Biol Chem. 276: 39765-39771. , Rutschman, R. J. (2003) SOCS3 regulates the plasticity of gp130 signaling, Nat Immunol. 4: 546-550. , Jove, R. & Yu, H. (2010) STAT3-induced S1PR1 expression is crucial for persistent STAT3 activation in tumors, Nat Med. 16: 1421-1428. M. & Yu, H. (2009) Persistently activated Stat3 maintains constitutive NF-kappaB activity in tumors, Cancer Cell.
This has led to the development of several biological drugs designed to block cytokine receptor activation by binding and sequestering free cytokine to prevent engagement with the cognate receptor, and each is typically administered either as part of a combination therapeutic regimen with one or more DMARDs or as monotherapy in patients not able to tolerate DMARD therapy or for whom it has proven ineffective. g. g. , 2010). , 2009). The development of IL-6 blockers came from a wealth of research implicating this pleiotropic cytokine in the progression of RA and other autoimmune conditions at several levels.