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AP1 (show FOSB ELISA Kits) binding sites were enriched upstream of genes up-regulated by TRAF3IP2 silencing. Correspondingly, nuclear expression of FosB (show FOSB ELISA Kits) and Fra1 (show FOSL1 ELISA Kits) was increased in TRAF3IP2-silenced cells. Many genes involved in host defense were induced by IL-17 (show IL17A ELISA Kits) in a TRAF3IP2-dependent fashion.
TRAF3IP2 SNP rs33980500 associated with no achievement of low disease activity nor remission at 6 months
the first report to describe a non-adaptor function of Act1 by directly binding to the promoter region of IL-17A (show IL17A ELISA Kits) responsive genes and directly regulate their transcription.
ACT1 is an essential adaptor molecule of Il-17 (show IL17A ELISA Kits)-induced expression of inflammation-related gene targets.
Both the ACT-1 assay and the MAdCAM-1 (show MADCAM1 ELISA Kits) assay demonstrated acceptable reproducibility and repeatability. The assays were sufficiently stable to allow for clinical use. During clinical testing the assays demonstrated that vedolizumab was able to saturate peripheral cells at all doses tested.
A G/G genotype of rs766748 in IL-17F (show IL17F ELISA Kits), and a C/C or C/A genotype of rs1883136 in TRAF3IP2.
The suppressive effects of miR (show MLXIP ELISA Kits)-30a were mediated by directly targeting Traf3ip2 mRNA
TRAF3IP2 may play a causal role in aldosterone-induced adverse cardiac remodeling in vivo.
Single nucleotide polymorphisms in RBPJ (show RBPJ ELISA Kits), IL1R1 (show IL1RN ELISA Kits), REV3L, TRAF3IP2, IRF1 (show IRF1 ELISA Kits) and ICOS (show CTLA4 ELISA Kits) showed association with rheumatoid arthritis in black South Africans.
A variant (rs76228616 SNP) in TRAF3IP2 gene could be involved in susceptibility to Steven-Johnson Syndrome.
TRAF3IP2 plays a causal role in atherosclerotic plaque development and vulnerability, possibly by inducing the expression of multiple proinflammatory mediators
TRAF3IP2 is a critical signaling intermediate in aldosterone/salt-induced myocardial hypertrophy and fibrosis, and thus a potential therapeutic target in hypertensive heart disease.
ameliorating myocardial damage by targeting TRAF3IP2 appears to be more effective to inhibiting its downstream signaling intermediates NF-kappaB (show NFKB1 ELISA Kits) and JNK (show MAPK8 ELISA Kits). Therefore, TRAF3IP2 could be a potential therapeutic target in ischemic heart disease
these results demonstrate that overexpression of TRAF3IP2 in male mice is sufficient to induce myocardial hypertrophy, cardiac fibrosis, and contractile dysfunction.
using massively parallel reporter assays, we dissect the enhancer activity of three liver eExons (SORL1 (show SORL1 ELISA Kits) exon 17, TRAF3IP2 exon 2, PPARG (show PPARG ELISA Kits) exon 6) at single nucleotide resolution in the mouse liver
TRAF3IP2 is a critical intermediate in IL-18 (show IL18 ELISA Kits)-induced cardiac fibroblast migration and differentiation in vitro.
Our results support the important role of Act1 in the regulation of self-reactive B cells and reveal how Act1 functions to prevent the production of autoantibodies.
These results demonstrate for the first time that AOPPs induce cardiomyocyte death via Nox2/Rac1/superoxide-dependent
CIKS knockdown inhibited high glucose-induced IKKbeta (show IKBKB ELISA Kits) and JNK (show MAPK8 ELISA Kits) phosphorylation, p65 (show NFkBP65 ELISA Kits) and c-Jun (show JUN ELISA Kits) nuclear translocation, and NF-kappaB (show NFKB1 ELISA Kits)- and AP-1 (show JUN ELISA Kits)-dependent proinflammatory cytokine, chemokine (show CCL1 ELISA Kits), and adhesion molecule (show NCAM1 ELISA Kits) expression.
The findings define a new role for the IKK-related kinases in suppressing IL-17-mediated NF-kappaB activation through TRAF6-dependent Act1 phosphorylation.
This gene encodes a protein involved in regulating responses to cytokines by members of the Rel/NF-kappaB transcription factor family. These factors play a central role in innate immunity in response to pathogens, inflammatory signals and stress. This gene product interacts with TRAF proteins (tumor necrosis factor receptor-associated factors) and either I-kappaB kinase or MAP kinase to activate either NF-kappaB or Jun kinase. Several alternative transcripts encoding different isoforms have been identified. Another transcript, which does not encode a protein and is transcribed in the opposite orientation, has been identified. Overexpression of this transcript has been shown to reduce expression of at least one of the protein encoding transcripts, suggesting it has a regulatory role in the expression of this gene.
NFkB-activating protein ACT1
, adapter protein CIKS
, connection to IKK and SAPK/JNK
, nuclear factor NF-kappa-B activator 1
, TRAF3 interacting protein 2
, adapter protein CIKS-like