Gene interactions and pathways from curated databases and text-mining

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MAP3K7 — NFKBIA

Pathways - manually collected, often from reviews:

  • KEGG Leishmaniasis: Complex of MAP3K7-TAB1-TAB2 → NFKBIA/NFKBIB (protein-protein, activation)
  • KEGG Measles: Complex of MAP3K7-TAB2 → NFKBIA/NFKBIB (protein-protein, activation)

Text-mined interactions from Literome

Shuto et al., Proc Natl Acad Sci U S A 2001 (MAP Kinase Signaling System) : Activation of NF-kappa B by nontypeable Hemophilus influenzae is mediated by toll-like receptor 2-TAK1 dependent NIK-IKK alpha /beta-I kappa B alpha and MKK3/6-p38 MAP kinase signaling pathways in epithelial cells
Chen et al., Biochem Biophys Res Commun 2004 : Nontypeable Haemophilus influenzae lipoprotein P6 induces MUC5AC mucin transcription via TLR2-TAK1 dependent p38 MAPK-AP1 and IKKbeta-IkappaBalpha-NF-kappaB signaling pathways ... Moreover, P6 induces MUC5AC transcription via TLR2-MyD88-IRAK1-TRAF6-TAK1 dependent p38 MAPK-AP1 and IKKbeta-IkappaBalpha-NF-kappaB signaling pathways
Haase et al., J Immunol 2005 (Yersinia Infections) : TAK1 is an important activator of the IkappaB kinase complex in the TLR signaling cascade
Sung et al., Mol Pharmacol 2007 : Fisetin, an inhibitor of cyclin dependent kinase 6, down-regulates nuclear factor-kappaB regulated cell proliferation, antiapoptotic and metastatic gene products through the suppression of TAK-1 and receptor interacting protein regulated IkappaBalpha kinase activation
Srivastava et al., J Biol Chem 2010 : Although both the TAK1 and the CARMA1 binding sites in ADAP are essential for IkappaB alpha phosphorylation and degradation and NF-kappaB nuclear translocation, only the TAK1 binding site in ADAP is necessary for IKK phosphorylation