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AP1 (show FOSB Proteins) binding sites were enriched upstream of genes up-regulated by TRAF3IP2 silencing. Correspondingly, nuclear expression of FosB (show FOSB Proteins) and Fra1 (show FOSL1 Proteins) was increased in TRAF3IP2-silenced cells. Many genes involved in host defense were induced by IL-17 (show IL17A Proteins) 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 Proteins) responsive genes and directly regulate their transcription.
ACT1 is an essential adaptor molecule of Il-17 (show IL17A Proteins)-induced expression of inflammation-related gene targets.
Both the ACT-1 assay and the MAdCAM-1 (show MADCAM1 Proteins) 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 Proteins), and a C/C or C/A genotype of rs1883136 in TRAF3IP2.
The suppressive effects of miR (show MLXIP Proteins)-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 Proteins), IL1R1 (show IL1RN Proteins), REV3L, TRAF3IP2, IRF1 (show IRF1 Proteins) and ICOS (show CTLA4 Proteins) 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 Proteins) and JNK (show MAPK8 Proteins). 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 Proteins) exon 17, TRAF3IP2 exon 2, PPARG (show PPARG Proteins) exon 6) at single nucleotide resolution in the mouse liver
TRAF3IP2 is a critical intermediate in IL-18 (show IL18 Proteins)-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 Proteins) and JNK (show MAPK8 Proteins) phosphorylation, p65 (show NFkBP65 Proteins) and c-Jun (show JUN Proteins) nuclear translocation, and NF-kappaB (show NFKB1 Proteins)- and AP-1 (show JUN Proteins)-dependent proinflammatory cytokine, chemokine (show CCL1 Proteins), and adhesion molecule (show NCAM1 Proteins) 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