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KRT13 — RELA
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