By G. Da Silva Xavier
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Extra info for Advances in Protein Kinases
R. & Cancer Genome Project (2005) Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders, Lancet. 365: 1054-1061. , Rose-John, S. F. (2004) TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling, Immunity. 21: 491-501. , Rose-John, S. F. (2007) IL-6 signaling promotes tumor growth in colorectal cancer, Cell Cycle. 4: 217-220. I. G. (2006) Stops along the RAS pathway in human genetic disease, Nat Med. 12: 283-285. , Gertler, A. & Monsonego-Ornan, E.
The different mechanisms by which STAT3 and NF-B (predominantly the RelA/p50 heterodimer) interact to enhance target gene transcription have been shown to be context-dependent but typically result in enhanced target gene induction. For example, Tyr705-phosphorylated STAT3 has been shown to bind promoter-bound RelA to facilitate the recruitment of the transcriptional co-activator p300, thereby triggering RelA acetylation. , 2009). , 2007). , 2007; Yang & Stark, 2008). While this phenomenon has only been studied in detail for the serum amyloid A gene mobilized as part of the acute phase response, it raises the possibility that NF-B/STAT3 complexes may be able to initiate a unique transcriptional programme, although any role in tumour progression is still unclear.
P. V. (2007) Tumor-suppressive activity of the cell death activator GRIM-19 on a constitutively active signal transducer and activator of transcription 3, Cancer Res. J. (2002) The role of transsignaling via the agonistic soluble IL-6 receptor in human diseases, Biochim Biophys Acta. 1592: 323-343. , Conaway, R. W. I. (2004) VHL-box and SOCS-box domains determine binding specificity for Cul2-Rbx1 and Cul5-Rbx2 modules of ubiquitin ligases, Genes Dev. 18: 3055-3065. C. W. (1998) The Elongin BC complex interacts with the conserved SOCS-box motif present in members of the SOCS, ras, WD-40 repeat, and ankyrin repeat families, Genes Dev.
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