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抗Human TRAF3IP2 抗体:
抗Mouse (Murine) TRAF3IP2 抗体:
抗Rat (Rattus) TRAF3IP2 抗体:
Human Polyclonal TRAF3IP2 Primary Antibody for 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 for 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 for 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 for 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
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.
Human IL-17A and IL-17F depend on ACT1 to mediate protective mucocutaneous immunity.
Data show the contribution of TRAF3IP2 genetic variability in Systemic lupus erythematosus (SLE) susceptibility.
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.
our findings indicate that Act1 expression in T cells is required for cellular and humoral Th2-mediated allergic responses and the development of airway hyperresponsiveness
IL-17-induced NF-kappaB activation via CIKS/Act1: physiologic significance and signaling mechanisms.
Study demonstrates that the TRAF3IP2 protein plays an important role in AD and suggests the protein as a therapeutic target to treat AD.
Data show that knockdown of TNFR-associated factor 6 or NF-kappaB activator 1 in 70Z/3 pre-B cells led to decreased Rgs16 expression, indicating that both of these two genes are involved in IL-17-mediated activation of NF-kappaB signaling in B cells.
Act1-deficient astrocytes showed impaired IL-17-mediated inflammatory gene induction; thus, astroctyes are critical in IL-17-Act1-mediated leukocyte recruitment during autoimmune-induced inflammation of the CNS
Whereas Act1 interacts with the IL-17R through the C-terminal SEFIR domain, Act1 is recruited to CD40 and BAFFR indirectly, which is mediated by TRAF3 through the TRAF binding site in Act1.
The impact of Act1 on both BAFF and CD40 pathways establishes Act1-deficient mice as a unique model to study distinct steps of autoimmunity and regulation of self tolerance.
ACT1/CIKS (formerly connection to IkappaB kinase and stress-activated protein kinases) is required for interleukin-25 induction of T helper type 2 (Th)2 cell cytokines, mucus hypersecretion, and airway hyperreactivity.
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