◀ Back to NFKB1

MKL1 — NFKB1

Text-mined interactions from Literome

Andreakos et al., Blood 2004 : We found that MyD88 and Mal/TIRAP are essential for LPS induced I kappa B alpha phosphorylation, NF-kappa B activation, and interleukin 6 (IL-6) or IL-8 production in fibroblasts and endothelial cells in a pathway that also requires IKK2 ... In contrast, in macrophages neither MyD88, Mal/TIRAP , nor I kappa B kinase 2 (IKK2) are required for NF-kappa B activation or tumor necrosis factor alpha (TNF alpha), IL-6, or IL-8 production, although Mal/TIRAP is still involved in the production of interferon beta (IFN beta)
Sacre et al., J Endotoxin Res 2004 : In cell lines and murine models, parts of the signaling pathways involved have been elucidated with MyD88, Mal/TIRAP and IKK2 playing an important role in the induction of NF-kappaB ... We show that in primary human macrophages MyD88, Mal/TIRAP and IKK2 independent alternative pathways activate NF-kappaB and induce the expression of inflammatory cytokines, whereas in non-myeloid synovial fibroblasts MyD88 and/or Mal/TIRAP are essential adaptors for LPS signaling
Verstak et al., J Biol Chem 2009 (Bacterial Infections...) : Furthermore, Mal interaction with TRAF6 mediates Ser phosphorylation of the p65 subunit of NF-kappaB and thus controls transcriptional activation but not nuclear translocation of NF-kappaB