High impact information on Traf3

• Mice homozygous with respect to the amn mutation generated by a transgene insertion have no amnion [1].
• Overexpression of a truncated CRAF1 gene inhibited CD40-mediated up-regulation of CD23 [2].
• It is likely that other members of the TNF receptor superfamily use CRAF-related proteins in their signal transduction processes [2].
• The CRAF1 sequence also predicted a long amphipathic helix, a pattern of five zinc fingers, and a zinc ring finger [2].
• Finally, we show that the early postnatal lethality observed in TRAF3-deficient mice is rescued by compound loss of the noncanonical NF-kappaB p100 gene [3].

Biological context of Traf3

• Importantly, TRAF3(-/-) B cells show ligand-independent up-regulation of intracellular adhesion molecule 1 and protection from spontaneous apoptosis during in vitro culture [3].
• To test whether CP8 contributes to the pathogenesis of S. aureus, we replaced the weak native promoter of the cap8 operon in strain Becker with the strong constitutive promoter of the cap1 operon of strain M [4].

Anatomical context of Traf3

• Traf2, Traf3 and Traf6 showed weak expression in the thickened epithelium [5].
• The amn gene product is required in extraembryonic tissues for the generation of middle primitive streak derivatives [6].

Associations of Traf3 with chemical compounds

• Role of TNF receptor-associated factor 3 in the CD40 signaling by production of reactive oxygen species through association with p40phox, a cytosolic subunit of nicotinamide adenine dinucleotide phosphate oxidase [7].

Regulatory relationships of Traf3

• In fact, TRAF3-deficient cells overproduce pro-inflammatory cytokines owing to defective IL-10 production [8].

Other interactions of Traf3

• Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6 [8].

References