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NFKBIA — SRC
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Hprd Interaction:
SRC
—
NFKBIA
(in vivo)
Fan et al., J Biol Chem 2003, Imbert et al., Cell 1996*, Abu-Amer et al., J Biol Chem 1998*
-
IRef Hprd Interaction:
SRC
—
NFKBIA
(in vitro)
Fan et al., J Biol Chem 2003, Imbert et al., Cell 1996*, Abu-Amer et al., J Biol Chem 1998*
Text-mined interactions from Literome
Fan et al., J Biol Chem 2003
(Anoxia) :
In vitro kinase assays further demonstrated that immunoprecipitated
c-Src has the capacity to directly phosphorylate GST-I kappa B alpha and that this
I kappa B alpha kinase activity is significantly
reduced by Gpx-1 overexpression ... These results suggest that
c-Src dependent tyrosine phosphorylation of
I kappa B alpha and subsequent activation of NF kappa B is controlled by intracellular H ( 2 ) O ( 2 ) and defines an important redox regulated pathway for NF kappa B activation following H/R injury that is independent of the IKK complex
Crèvecoeur et al., Biochem Pharmacol 2008
:
In the present study, we investigated the effect of GA on NF-kappaB activation induced by sodium pervanadate ( PV ), a tyrosine phosphatase inhibitor triggering
c-Src mediated tyrosine phosphorylation of
IkappaBalpha
Abu-Amer et al., J Biol Chem 1998
:
Consistent with the pivotal role
played by
c-Src in TNF induced
Ikappa Balpha tyrosine phosphorylation, NF-kappaB activation, by the cytokine, is markedly delayed and reduced in c-src-/- BMMs. Underscoring the physiological significance of c-Src activation of NF-kappaB, TNF induction of IL-6, which is an NF-kappaB mediated event, is substantially diminished in c-src-/- BMMs