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anti-Human TRAF3IP2 Antikörper:
anti-Mouse (Murine) TRAF3IP2 Antikörper:
anti-Rat (Rattus) TRAF3IP2 Antikörper:
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Human Polyclonal TRAF3IP2 Primary Antibody für IHC (p), SimWes - ABIN4361705
Valente, Yoshida, Clark, Delafontaine, Siebenlist, Chandrasekar: Advanced oxidation protein products induce cardiomyocyte death via Nox2/Rac1/superoxide-dependent TRAF3IP2/JNK signaling. in Free radical biology & medicine 2013
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Human Polyclonal TRAF3IP2 Primary Antibody für IHC (p), WB - ABIN541423
Li, Commane, Nie, Hua, Chatterjee-Kishore, Wald, Haag, Stark: Act1, an NF-kappa B-activating protein. in Proceedings of the National Academy of Sciences of the United States of America 2000
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Human Polyclonal TRAF3IP2 Primary Antibody für IHC (p), WB - ABIN541422
Leonardi, Chariot, Claudio, Cunningham, Siebenlist: CIKS, a connection to Ikappa B kinase and stress-activated protein kinase. in Proceedings of the National Academy of Sciences of the United States of America 2000
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Human Polyclonal TRAF3IP2 Primary Antibody für ELISA, WB - ABIN4361709
Qian, Liu, Hartupee, Altuntas, Gulen, Jane-Wit, Xiao, Lu, Giltiay, Liu, Kordula, Zhang, Vallance, Swaidani, Aronica, Tuohy, Hamilton, Li: The adaptor Act1 is required for interleukin 17-dependent signaling associated with autoimmune and inflammatory disease. in Nature immunology 2007
We also identify a novel LRI site located within the TRAF3IP2-AS1 promoter, 200 kb distant from the TRAF3IP2 promoter, showing genetic association with psoriasis both in our discovery cohort, as well as in the large WTCCC replication cohort.
Act1 D10N missense mutation impairs CD40L-induced phosphorylation of p65, p38, and Erk in B-cells.
Four genes-ACT1, PIN1, DNMT1 and NTN1-emerged as having roles in pathways that may influence Primary Biliary Cholangitis pathogenesis in British Columbia First Nations people.
AP1 binding sites were enriched upstream of genes up-regulated by TRAF3IP2 silencing. Correspondingly, nuclear expression of FosB and Fra1 was increased in TRAF3IP2-silenced cells. Many genes involved in host defense were induced by IL-17 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 responsive genes and directly regulate their transcription.
ACT1 is an essential adaptor molecule of Il-17-induced expression of inflammation-related gene targets.
Both the ACT-1 assay and the MAdCAM-1 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, and a C/C or C/A genotype of rs1883136 in TRAF3IP2.
The suppressive effects of miR-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, IL1R1, REV3L, TRAF3IP2, IRF1 and ICOS 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.
identify Syk as an upstream signaling molecule in IL-17A-induced Act1-TRAF6 interaction in keratinocytes, and inhibition of Syk can attenuate CCL20 production
These results indicate that oxLDL-induced endothelial cell death and dysfunction are mediated via TRAF3IP2 and that native HDL3 and the AMPK activators inhibit this response.
Replicate the association of TRAF3IP2-_rs33980500 variant with the susceptibility to psoriasis.
this study demonstrated that although ACT1-v2-D10N is nonfunctional, ACT1-v1-D19N retains the ability to interact with Hsp90 and is fully responsive to IL-17A stimulation.
Genetic polymorphism in the TRAF3IP2 gene is associated with psoriasis vulgaris in a Japanese population.
This study provides evidence that TRAF5 and TRAF3IP2 genes are involved in the development ofBehcet's disease (BD) and Vogt-Koyanagi-Harada (VKH) syndrome.
Results suggest that Act1 might play a key role in the pathophysiology and the treatment of rheumatoid arthritis.
Act1 is a negative regulator in T and B cells via direct inhibition of STAT3.
Study shows that miR-215 regulates the Act1/IL-17RA pathway and represses the expression of Act1 protein in oxygen glucose deprivation/reperfusion-treated N2a cells and an middle cerebral artery occlusion mouse model of ischemic stroke.
knock-out mice develop spontaneous IL-22-dependent skin inflammation
Targeted Act1 deficiency in epithelial cells resulted in a marked delay in worm expulsion.
IL-17 mediates estrogen-deficient osteoporosis in an Act1-dependent manner.
Act1 adaptor protein is an immediate and essential signaling component of interleukin-17 receptor
Confirming its critical role in TWEAK signaling, silencing TRAF3IP2 inhibited TWEAK autoregulation, TWEAKR upregulation, p38 MAPK, NF-kappaB and AP-1 activation, inflammatory cytokine expression, MMP and TIMP1 activation, collagen expression and secretion, and importantly, proliferation and migration
These results reveal a network in which Act1 assembles RNA-protein complexes on the 3' UTRs of select mRNAs and consequently controls receptor-mediated mRNA stabilization and translation during inflammation
Inhibition of DPP-4 activity by linagliptin reverses Western diet-induced diastolic dysfunction, possibly by targeting TRAF3IP2 expression and its downstream inflammatory signaling.
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 and JNK. 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 exon 17, TRAF3IP2 exon 2, PPARG exon 6) at single nucleotide resolution in the mouse liver
TRAF3IP2 is a critical intermediate in IL-18-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 and JNK phosphorylation, p65 and c-Jun nuclear translocation, and NF-kappaB- and AP-1-dependent proinflammatory cytokine, chemokine, and adhesion molecule 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 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