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NFKB1 — SOAT1

Text-mined interactions from Literome

Knecht et al., Oncology 2001 (Cell Transformation, Neoplastic...) : TRAF2 mediated NF-kappaB activation, AP-1 induction and JAK3/STAT activation may result in sustained proliferation leading to lymphoma
Nakamura et al., J Biol Chem 2002 (MAP Kinase Signaling System) : In addition, STAT5 dependent NF-kappa B activation is mediated not through an inducible nuclear translocation but via up-regulation of both DNA binding activity and transactivation potential of NF-kappa B
Rothfuchs et al., J Immunol 2004 : Such NF-kappaB activation was independent of IFN-alphabeta, STAT1 , and RNA dependent protein kinase
Nishinakamura et al., Int Immunol 2007 : Thus, STAT3C could suppress the transcriptional and/or translational activity of NF-kappaB
Hu et al., J Leukoc Biol 2007 : Similarly, basal ITAM signaling augments IFN signaling and function of receptor activator of NF-kappaB , but extensive ITAM activation inhibits Jak-STAT signaling
Kim et al., PLoS Biol 2007 : We conclude that an inhibitory effect of AP-1 and STAT on NF-kappaB is required for properly balanced immune responses and appears to be evolutionarily conserved
Han et al., Molecular cancer 2010 (Disease Models, Animal...) : Co-treatment with NF-kappaB , STAT3 or/and PI3K inhibitors led to additive inhibition of iMyc E mu-1 cell proliferation, suggesting that these signaling pathways converge