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RELA — SRC
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Wooten et al., Mol Cell Biol 2000
:
Src , PI3K, and PKC-iota were likewise
required for NGF induced
NF-kappaB activation and cell survival, whereas Ras was not required for either survival or NF-kappaB activation but was required for differentiation ... Consistent with a
role for
Src in regulating
NF-kappaB activation, an absence of Src activity impaired recruitment of PKC-iota into an IKK complex and markedly impaired NGF induced translocation of p65/NF-kappaB to the nucleus
Sakai et al., J Biochem 2001
:
Receptor activator of
NF-kappaB ( RANKL ) significantly
increased the LBC levels of cathepsin K, TRAP, and
c-Src , whereas calcitonin decreased the LBC levels of cathepsin K, TRAP, and Rab7, indicating that the transformation of early to late endosomal elements and lysosomes in OCLs is also regulated by osteoclastogenesis regulatory factors
Fan et al., J Biol Chem 2003
(Anoxia) :
In the present study, we investigated the
involvement of
c-Src in the redox activation of
NFkappaB following H/R or pervanadate treatment ... 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
Funakoshi-Tago et al., Eur J Biochem 2003
:
We found that IL-1 mediated
c-Src activation was
required for AP-1 activation, but not for
NF-kappa B activation and also revealed that c-Src induced AP-1 activation was enhanced synergistically by the coexpression of TNF receptor associated factor 6 (TRAF6)
Yang et al., Mol Pharmacol 2003
:
Activation of D2R led to phosphorylation of c-Src at Tyr-418, and expression of a kinase-deficient
c-Src inhibited D2R mediated
NF-kappaB activation ... These results suggest that D2R mediated
NF-kappaB activation
requires Gbetagamma and
c-Src , and possibly involves beta-arrestin 1
Lerner-Marmarosh et al., Arterioscler Thromb Vasc Biol 2003
(Inflammation) :
TNF-alpha mediated JNK, c-Jun, and
NF-kappaB activation
required Src and SHP-2 activity
Jalal et al., J Am Soc Nephrol 2006
:
Src activation of
NF-kappaB augments IL-1beta induced nitric oxide production in mesangial cells ... In agreement with the pharmacologic inhibition studies, siRNA directed against c-Src specifically limited
c-Src protein expression and
inhibited IL-1beta mediated induction of
NF-kappaB DNA binding activity, whereas control siRNA had no effect ... Conversely, overexpression of constitutively active
c-Src augmented basal and IL-1beta mediated induction of
NF-kappaB DNA binding activity and NO production
Heinemann et al., J Biol Chem 2006
(Cell Transformation, Viral) :
NFkappaB induction by Tio is
independent of
Src-kinase interaction and tyrosine phosphorylation of Tio
Trevino et al., Angiogenesis 2006
(Adenocarcinoma...) :
Pharmacologic inhibition of
NF-kappaB activity significantly reduced basal IL-8 expression and tumor necrosis factor induced IL-8 expression ( P < 0.05 for both ), yet NF-kappaB activity was not
dependent on
Src
Salanova et al., J Biol Chem 2007
:
We show that
Src and Syk non-receptor tyrosine kinases, as well as the actin cytoskeleton,
control NF-kappaB activation
Li et al., Biochem J 2008
:
c-Src has been shown to
activate NF-kappaB ( nuclear factor kappaB ) following H/R ( hypoxia/reoxygenation ) by acting as a redox dependent IkappaBalpha ( inhibitory kappaB ) tyrosine kinase
Hsieh et al., Biochim Biophys Acta 2008
:
Moreover, thrombin stimulated
activation of
NF-kappaB , AP-1, and COX-2 promoter activity was blocked by the inhibitors of
c-Src , PKC, EGFR, MEK1/2, AP-1 and NF-kappaB, suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Pincheira et al., J Immunol 2008
:
TNFR1/c-Src , but not TNFR1/Jak2,
plays an obligate role in the activation of
NF-kappaB by TNF, whereas TNFR1/Jak2, but not TNFR1/c-Src, plays an obligate role in the activation of STAT3
Fan et al., J Biol Chem 2009
(MAP Kinase Signaling System...) :
Src enhanced basal and SF stimulated
NF-kappaB activity and SF protection against ADR, in a manner dependent upon its kinase and Src homology 3 domains ; and endogenous
Src was
required for SF stimulation of NF-kappaB activity and cell protection ... The ability of Src to enhance SF stimulation of NF-kappaB activity was due, in part, to its ability to stimulate Akt and IkappaB kinase activity ; and
Src mediated stimulation of
NF-kappaB was due, in part, to a Rac1/MKK3/6/p38 pathway and was Akt dependent ... The NF-kappaB inducing kinase was found to act downstream of TAK1 ( transforming growth factor-beta activated kinase 1 ) as a mediator of SF- and
Src stimulated
NF-kappaB activity
Hsieh et al., Neurotox Res 2010
:
Taken together, these results suggested that in RBA-1 cells,
activation of
NF-kappaB by a
c-Src dependent PI3K/Akt-p42/p44 MAPK activation mediated through transactivation of PDGFR is essential for MMP-9 gene upregulation induced by LTA
Boukerche et al., Oncogene 2010
(Melanoma) :
MDA-9/syntenin also promotes melanoma metastasis by activating c-Src, but how
c-Src regulates
NF-kappaB activation is unclear ... Inhibition of
c-Src by PP2 treatment, by blocking c-Src or mda-9/syntenin expression with small interfering RNA, or in c-Src ( -/- ) knockout cell lines,
reduces NF-kappaB activation following overexpression of mda-9/syntenin or c-Src
Scatena et al., J Cell Biol 1998
:
Activation of NF-kappaB by osteopontin depended on the small GTP binding protein Ras and the tyrosine kinase Src, since
NF-kappaB reporter activity was
inhibited by Ras and
Src dominant negative mutants
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