◀ Back to RELA
RELA — STS
Text-mined interactions from Literome
Manji et al., J Biol Chem 2002
:
When expressed in cells,
ASC recruits PYPAF1 to distinct cytoplasmic loci and
induces the activation of
NF-kappaB ... Furthermore, coexpression of PYPAF1 with
ASC results in a potent synergistic activation of
NF-kappaB ... These findings suggest that PYPAF1 and
ASC function as upstream
activators of
NF-kappaB signaling
Feng et al., Am J Physiol Gastrointest Liver Physiol 2002
(Necrosis) :
STS activated
I kappa B kinase and nuclear factor-kappa B (NF-kappa B) nuclear translocation and DNA binding but inhibited transactivation of I kappa B-alpha, inducible nitric oxide synthase, and inhibitor of apoptosis protein-1 in hepatocytes and NF-kappa B reporter in transfected Huh-7 cells ...
STS activated I kappa B kinase and
nuclear factor-kappa B (NF-kappa B) nuclear translocation and DNA binding but inhibited transactivation of I kappa B-alpha, inducible nitric oxide synthase, and inhibitor of apoptosis protein-1 in hepatocytes and NF-kappa B reporter in transfected Huh-7 cells
Grenier et al., FEBS Lett 2002
:
Co-expression of PYPAF5 with
ASC results in a synergistic activation of
NF-kappaB and the recruitment of PYPAF5 to punctate structures in the cytoplasm
Stehlik et al., J Exp Med 2002
:
While coexpression of
ASC with certain PAAD-family proteins such as Pyrin and Cryopyrin
increases NF-kappaB activity, ASC has an inhibitory influence on NF-kappaB activation by various proinflammatory stimuli, including tumor necrosis factor (TNF)alpha, interleukin 1beta, and lipopolysaccharide (LPS)
Dowds et al., Biochem Biophys Res Commun 2003
(Familial Mediterranean Fever) :
Notably, pyrin, the product of the familial Mediterranean fever gene,
inhibited cryopyrin mediated apoptosis and
NF-kappaB activation by disrupting the
cryopyrin-ASC interaction
Stehlik et al., Biochem J 2003
:
In gene transfer experiments,
POP1/ASC2 suppressed cytokine mediated
NF-kappa B activation similar to other PAAD-family proteins previously tested
Hasegawa et al., J Biol Chem 2005
(Inflammation) :
ASC mediated
NF-kappaB activation leading to interleukin-8 production requires caspase-8 and is inhibited by CLARP ... The catalytic activity of caspase-8 was required for the
ASC mediated
NF-kappaB activation when caspase-8 was expressed at an endogenous level, although it was not essential when caspase-8 was overexpressed ... These results are the first to indicate that caspase-8 plays an important role in the ASC mediated
NF-kappaB activation, and that the
ASC mediated NF-kappaB activation actually
induces physiologically relevant gene expression
Saito et al., Arthritis Rheum 2005
(Chronic Disease...) :
In addition, the Y570C mutation ( with or without the S196N polymorphism ) increased the ability of CIAS1 to induce
ASC dependent
NF-kappaB activation, unlike the wild-type gene or the gene bearing the S196N polymorphism alone ... The production of interleukin-1beta (IL-1beta) by peripheral blood mononuclear cells ( PBMCs ) was measured by enzyme linked immunosorbent assay, and the ability of the mutant CIAS1 gene to enhance
ASC dependent
NF-kappaB activation was assessed to confirm that the mutations of CIAS1 found were responsible for the patient 's clinical manifestations of the CINCA syndrome
Sarkar et al., J Immunol 2006
:
This RIP2 induced
NF-kappaB activity and caspase-1 binding was
inhibited in a dose dependent fashion by
ASC
Kinoshita et al., Int Immunol 2006
:
When co-expressed in HEK293 cells, FAF1 interfere with the
NF-kappaB activation
induced by PYPAF1 and
ASC
Hasegawa et al., J Immunol 2009
:
Although the role of ASC in caspase-1 mediated IL-1beta and IL-18 maturation is well known,
ASC also
induces NF-kappaB activation and cytokine gene expression in human cells
Imamura et al., J Immunol 2010
(Shock, Septic) :
Interestingly, the NOD of human PYNOD was sufficient to inhibit caspase-1 mediated IL-1beta secretion, whereas its pyrin domain was sufficient to inhibit
ASC mediated
NF-kappaB activation and apoptosis and to reduce ASC 's ability to promote caspase-1 mediated IL-1beta production