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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