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KRT13 — NFKB1

Text-mined interactions from Literome

Matta et al., J Biol Chem 2003 : We demonstrate that receptor interacting protein and NF-kappaB inducing kinase are dispensable for vFLIP K13 induced NF-kappaB DNA binding and transcriptional activation ... On the other hand, vFLIP K13 induced NF-kappaB DNA binding activity is significantly reduced, although not absent, in cells deficient in IKK1, IKK2, and NEMO ... Furthermore, vFLIP K13 induced NF-kappaB transcriptional activity is only weakly present in IKK1-deficient cells and almost completely absent in those deficient in IKK2 and NEMO ... HHV8 vFLIP K13 induced NF-kappaB activation in IKK1- and IKK2-deficient fibroblasts could be rescued by wild type but not by the kinase-inactive mutants of IKK1 and IKK2, respectively ... Consistent with the above results, vFLIP K13 induced NF-kappaB activation could be effectively blocked by chemical inhibitors of the kinase activity of IKK1 and IKK2 ... Thus, a cooperative interaction of all three subunits of the IKK complex is required for maximal NF-kappaB activation via HHV8 vFLIP K13 ... Selective inhibitors of the IKK1 kinase activity may have a role in the treatment of disorders caused by abnormal NF-kappaB activation by HHV8 vFLIP K13
Matta et al., J Biol Chem 2007 : The K13-TRAF2 interaction is believed to be essential for the recruitment of K13 to the I-kappaB kinase (IKK) complex and for K13 induced NF-kappaB and JNK activation ... In addition, TRAF3 has been reported to be required for K13 induced NF-kappaB and JNK activation ... Furthermore, endogenously expressed TRAF2 and TRAF3 do not interact with K13 and play no role in K13 induced NF-kappaB activation or its interaction with the IKK complex ... Selective NF-kappaB activation by K13 might represent a novel strategy employed by the virus to promote latency
Matta et al., Oncogene 2008 (Sarcoma, Kaposi) : However, neither the IKKs nor NF-kappaB activation is required for nuclear localization of K13
Thurau et al., J Virol 2009 : The induction of MnSOD expression was dependent on vFLIP/K13 mediated activation of NF-kappaB , occurred in a cell-intrinsic manner, and was correlated with decreased intracellular superoxide accumulation and increased resistance of endothelial cells to superoxide induced death
Punj et al., Oncogene 2010 (Sarcoma, Kaposi) : Our results show that K13 induced NF-kappaB activity suppresses CXCR4 through upregulation of miR-146a