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AP1 (zeige FOSB ELISA Kits) binding sites were enriched upstream of genes up-regulated by TRAF3IP2 silencing. Correspondingly, nuclear expression of FosB (zeige FOSB ELISA Kits) and Fra1 (zeige FOSL1 ELISA Kits) was increased in TRAF3IP2-silenced cells. Many genes involved in host defense were induced by IL-17 (zeige 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 (zeige IL17A ELISA Kits) responsive genes and directly regulate their transcription.
ACT1 is an essential adaptor molecule of Il-17 (zeige IL17A ELISA Kits)-induced expression of inflammation-related gene targets.
Both the ACT-1 assay and the MAdCAM-1 (zeige 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 (zeige IL17F ELISA Kits), and a C/C or C/A genotype of rs1883136 in TRAF3IP2.
The suppressive effects of miR (zeige 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 (zeige RBPJ ELISA Kits), IL1R1 (zeige IL1RN ELISA Kits), REV3L, TRAF3IP2, IRF1 (zeige IRF1 ELISA Kits) and ICOS (zeige 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 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 (zeige NFKB1 ELISA Kits) and JNK (zeige 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 (zeige SORL1 ELISA Kits) exon 17, TRAF3IP2 exon 2, PPARG (zeige PPARG ELISA Kits) exon 6) at single nucleotide resolution in the mouse liver
TRAF3IP2 is a critical intermediate in IL-18 (zeige 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 (zeige IKBKB ELISA Kits) and JNK (zeige MAPK8 ELISA Kits) phosphorylation, p65 (zeige NFkBP65 ELISA Kits) and c-Jun (zeige JUN ELISA Kits) nuclear translocation, and NF-kappaB (zeige NFKB1 ELISA Kits)- and AP-1 (zeige JUN ELISA Kits)-dependent proinflammatory cytokine, chemokine (zeige CCL1 ELISA Kits), and adhesion molecule (zeige 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.
Data show that deletion of the CC' loop from Act1 or IL-17RA (zeige IL17RA ELISA Kits) abolished the interaction between both proteins.
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