TRAF3

A gene on chromosome 14q32.32 that encodes TNF receptor-associated factor 3, which regulates NF-kappaB kinase and MAP kinase activation, plays a central role in regulating B-cell survival, and is part of signalling pathways leading to cytokine and interferon production. TRAF3 is required for normal antibody isotype switching from IgM to IgG, and it plays a role in T-cell dependent immune responses as well as antiviral responses. It is an essential constituent of several E3 ubiquitin-protein ligase complexes and may promote Lys-63-linked ubiquitination of target proteins. It inhibits NF-kappaB activation in response to LTBR stimulation, as well as TRAF2-mediated NF-kappaB activation, and it downregulates proteolytic processing of NFKB2 and NF-kappaB activation. It promotes ubiquitination and proteasomal degradation of MAP3K14.

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References in periodicals archive

pylori infection exhibited higher levels of Cdx2 expression and lower levels of TRAF3 expression than those of NOD1-intact mice.

Nucleotide-binding oligomerization domain 1 and gastrointestinal disorders

In addition, differentially expressed genes involved mainly in molecular functions were mainly related to protein binding, Hsa04620: toll-like rece 8 0.45% RAC1, TRAF3, MAPK3, IFNAR1,0.00002 signaling pathway TICAM1, IL6, MAPK11, and IFNA1 nucleic acid binding, structure-specific DNA binding, RNA binding, and hexosaminidase activity.

Whole genome expression profiling and signal pathway screening of MSCs in ankylosing spondylitis

Scientists at The University of Texas MD Anderson Cancer Center, Houston, have identified TRAF3's savior and demonstrated how it works.

Pivotal enzyme rescued by another molecule

Then, MAVS is positioned on the mitochondrial outer membrane and recruits TRAF3, which can phosphorylate IRF3/IRF7 (IFN regulatory factor) when ubiquitin is terminated which starts the type I IFN antiviral immune response [34].

Toll-Like Receptors and RIG-I-Like Receptors Play Important Roles in Resisting Flavivirus

Meanwhile, TRIF also activates TRAF3 which recruits IKK-related kinases (TBK1 and IKKe) and IKK[gamma] for IRF3 phosphorylation, which translocates into the nucleus inducing the expression of type IIFN genes [2, 41].

The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism

The stimulation of TLR7 and TLR9 with their respective ligand results in the formation of a complex constituted by MyD88, IRAK-4, TRAF6, TRAF3, IRAK-1, IKK-[kappa], and IRF7 re sponsible for the activation of IRF7, which once phosphorylated is translocated to the nucleus and regulates the expression of type-I IFN.

Reconocimiento viral por el sistema inmune innato: papel de los receptores de reconocimiento de patrones

This occurs through IRF7 activation by IRAK-1 phosphorylation in a MyD88, IRAK-1, TRAF3, IKK[alpha], and IRK7 complex [77].

TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling

The cytoplasmic domain of Fn14 contains a phylogenetically conserved binding motif, and TRAF1, TRAF2, TRAF3, and TRAF5 are able to bind to this site [3].

TWEAK/Fn14 Activation Participates in Skin Inflammation

Recently it has been published that TRAF-2 controls the fate of IRF5 and c-Rel by proteasomal degradation via TRAF3 and cIAP.

Inflammation and Cancer: Extra- and Intracellular Determinants of Tumor-Associated Macrophages as Tumor Promoters