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Validated All-in-One™ qPCR Primer for TRAF3(NM_145725.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene is a member of the TNF receptor associated factor (TRAF) protein family. TRAF proteins associate with, and mediate the signal transduction from, members of the TNF receptor (TNFR) superfamily. This protein participates in the signal transduction of CD40, a TNFR family member important for the activation of the immune response. This protein is found to be a critical component of the lymphotoxin-beta receptor (LTbetaR) signaling complex, which induces NF-kappaB activation and cell death initiated by LTbeta ligation. Epstein-Barr virus encoded latent infection membrane protein-1 (LMP1) can interact with this and several other members of the TRAF family, which may be essential for the oncogenic effects of LMP1. Three alternatively spliced transcript variants encoding two distinct isoforms have been reported. [provided by RefSeq].
Gene References into function
- The TRAF domain from TRAF3 has been crystallized.
- Lymphotoxin beta receptor induces interleukin 8 gene expression via NF-kappaB and AP-1 activation.(AP-1)
- results suggest that in DG75 cells, TRAF3-induced MEK1 activation may be involved in CD40-mediated upregulation of IL-4-driven germline C epsilon transcription
- Results establish a major role of TRAF3 and -6 in X-linked ectodermal dysplasia receptor (XEDAR) signaling and in the process of ectodermal differentiation.
- TRAF3 interacts with BAFFR in yeast two-hybrid assays and in TALL-1-treated B lymphoma cells and is a negative regulator of BAFFR-mediated NF-kappa B activation and IL-10 production.
- TRAF2, TRAF3, cIAP1, Smac, and lymphotoxin beta receptor associate and are involved in apoptosis
- EBV LMP1 blocks p16INK4 pathway by promoting nuclear export of E2F-4 and E2F-5.
- the TRAF3-binding crevice has hot spots that promote molecular interactions driving specific signaling after contact with LTbetaR, CD40, or the downstream regulator TANK
- LMP1 associated protein induces micronucleus formation, represses DNA repair and enhances sensitivity to DNA-damaging agents in human epithelial cells.
- induction of noncanonical NF-kappaB signaling may involve the rescue of NIK from TRAF3-mediated negative regulation
- there is a novel association between TRAF2 and TRAF3 that is mediated by unique portions of each protein and that specifically regulates activation of NF-kappaB, but not AP-1
- LMP-1 proteins are required for in vitro growth of non-Hodgkin lymphoma cells.
- This study of the crystal structure of TRAF3 bound in complex with BAFF-R reveals the dynamic conformational adjustment of Tyr377 in TRAF3 that occurs forming a new intermolecular contact with BAFF-R that stabilizes the complex.
- TRAF3 specifically blocked the NF-kappaB activation via TRAF2/5.
- LMP1 from the Epstein-Barr virus is a structural CD40 decoy in B lymphocytes for binding to TRAF3.
- LMP1 utilizes two distinct pathways to activate NF-kappaB: a major one through CTAR2/TRAF6/TAK1/IKKbeta (canonical pathway) and a minor one through CTAR1/TRAF3/NIK/IKKalpha (noncanonical pathway)
- These data indicate that vFLIP uses TRAF2 and TRAF3 for signalling to NF-kappaB, which is crucial for KSHV-associated lymphomagenesis
- TRAF3 stabilization, JNK activation and caspase-9 induction define a novel pathway of CD40-mediated apoptosis in carcinoma cells.
- TRAF3 has a role in innate antiviral immunity [review]
- TRAF3, like Cardif, is required for type I interferon production in response to intracellular double-stranded RNA.
- The current data support the notion that LMP1 modifies stress-induced apoptosis in epithelial cells through molecular interactions downstream of its C-terminal signaling domain.
- Results show that decrease in the ubiquitination of TRAF3 is YopJ-dependent and to prevent or is to remove the K63-polymerized ubiquitin conjugates required for signal transduction.
- Dominant-negative forms of TRAF2 and TRAF3 inhibited but did not fully block LMP1-mediated transformation.
- Inactivation of TRAF3 is associated with multiple myeloma
- LMP1's activation of the unfolded protein response is a normal event in a continuum of LMP1's expression that leads both to stimulatory and inhibitory functions and regulates the physiology of epstein barr virus-infected B cells.
- The researchers found an association between LMP1 30-bp deletion or XhoI-loss with Chinese race and type III nasopharyngeal carcinoma.
- Somatic mutation of TRAF3 gene is rare in common human cancers and acute leukemias.
- These findings indicate that the NY-1V Hantavirus Gn cytoplasmic tail forms a complex with TRAF3 which disrupts the formation of TBK1-TRAF3 complexes and downstream signaling responses required for IFN-beta transcription.