◀ Back to NFKB1

NFKB1 — UGCG

Text-mined interactions from Literome

Manna et al., Oncogene 1999 : gamma-GCS overexpression also completely suppressed NF-kappa B activation induced by phorbol ester and okadaic acid, whereas that induced by H2O2, ceramide, and lipopolysaccharide was minimally affected
Braun et al., Neurosci Lett 2000 : GCs can suppress the activity of the redox-sensitive nuclear factor NF-kappaB , which potentially serves neuroprotective functions
Kawakita et al., Biol Pharm Bull 2003 : The effect of inhibitors of activator protein-1 (AP-1) and nuclear factor kappaB (NF-kappaB) on the radiation induced gamma-GCS gene expression was then examined
Hofmann et al., Biol Chem 2002 : While the biochemical mechanisms mediating repression of NF-kappaB activity by glucocorticoids (GCs) are relatively well studied, the role of promoter architecture for the effects of GCs on NF-kappaB remains poorly characterized
Muroya et al., Biochem Biophys Res Commun 2003 : We found that the nuclear factor-kappaB (NF-kappaB) mediated induction of gamma-GCS by LPS ( 100 ng/ml ) was suppressed by a 48-h pre-treatment with oxLDL ( 50 micro/ml ), and this was due to a decrease in the DNA binding activity of NF-kappaB ... Together, these indicate that oxidative modification of NF-kappaB suppresses LPS induced expression of gamma-GCS gene in ox-LDL treated cells, suggesting an implication of oxLDL induced modulation of NF-kappaB signaling with atherosclerosis
Morante et al., Free radical research 2005 (Body Weight...) : Moreover, chromatin immunoprecipitation ( ChIP ) assay demonstrated that NF-kappaB directly regulates transcription of gamma-GCS ( both subunits ) and cyclin D1 through the binding of NF-kappaB to the corresponding gene promoters, which was enhanced in vitamin E-deficiency
Ray et al., Biochem J 1997 : Evidence that GCs also inhibited cytokine activation of a synthetic nuclear factor kappaB (NFkappaB)-driven reporter gene transiently transfected into A549 cells suggested that interference with the activation and/or function of this transcription factor was important for GC inhibition of ESAP