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RELA — SOCS3
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 *
Text-mined interactions from Literome
Park et al., DNA Cell Biol 2003
:
Here we examined the
effects of
SOCS-3 on
NF-kappaB activity ... Analysis of C-terminal truncation mutants of SOCS-1 and SOCS-3 demonstrated that the SOCS box and its N-terminal region, a less well conserved linker region were important for
SOCS-3 activation of
RelA
Karlsen et al., Diabetologia 2004
:
Multiple IL-1beta induced NF-kappaB dependent proapoptotic early response genes were inhibited by SOCS-3 expression, suggesting that
SOCS-3 inhibits
NF-kappaB mediated signalling
Ohishi et al., J Immunol 2005
(Bone Resorption) :
These data suggest that both SOCS1 and
SOCS3 regulate osteoclastogenesis by blocking the inhibitory effect of inflammatory cytokines on receptor activator of the
NF-kappaB ligand mediated osteoclast differentiation signals
Spangenburg et al., J Physiol 2006
:
SOCS-3 overexpression
increased NF-kappaB transcriptional activity by 27-fold
Frobøse et al., Mol Endocrinol 2006
:
Suppressor of cytokine signaling
(SOCS)-3 was shown to
inhibit IL-1 induced transcription and activation of
NFkappaB and the MAPKs JNK and p38, but the mechanism is unknown
Pauli et al., PLoS Pathog 2008
:
Influenza A virus inhibits type I IFN signaling via
NF-kappaB dependent induction of
SOCS-3 expression
Akhtar et al., J Immunol 2010
(AIDS Dementia Complex...) :
In vitro, the HIV-1 regulatory protein transactivator of transcription induces
SOCS3 in human and murine macrophages in a
NF-kappaB dependent manner
Usui et al., Nihon rinsho. Japanese journal of clinical medicine 2011
(Diabetes Mellitus, Type 2...) :
These inflammatory mediators inhibit insulin signaling with several mechanisms, such as serine-phosphorylation of IRS-1, the induction of
SOCS3 and the
activation of JNK or
NFkappaB signaling in insulin-target tissues