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TRAF3IP2 encodes a protein involved in regulating responses to cytokines by members of the Rel/NF-kappaB transcription factor family. Additionally we are shipping TRAF3IP2 Antibodies (117) and many more products for this protein.
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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.
identify Syk (show SYK Proteins) as an upstream signaling molecule in IL-17A (show IL17A Proteins)-induced Act1-TRAF6 (show TRAF6 Proteins) interaction in keratinocytes, and inhibition of Syk (show SYK Proteins) can attenuate CCL20 (show CCL20 Proteins) production
These results indicate that oxLDL-induced endothelial cell death and dysfunction are mediated via TRAF3IP2 and that native HDL3 and the AMPK (show PRKAA1 Proteins) 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 (show HSP90 Proteins) and is fully responsive to IL-17A (show IL17A Proteins) stimulation.
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.
Data show that deletion of the CC' loop from Act1 or IL-17RA (show IL17RA Proteins) 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 (show IL17A Proteins)-induced NF-kappaB (show NFKB1 Proteins) 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.
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.
adapter protein CIKS
, TRAF3 interacting protein 2
, adapter protein CIKS-like
, NFkB-activating protein ACT1
, connection to IKK and SAPK/JNK
, nuclear factor NF-kappa-B activator 1