Disease relevance of Traf2

• To examine whether TRAF2 overexpression induced osteoclastogenesis, TRAF2 was overexpressed in osteoclast progenitors form wildtype bone marrow by retrovirus infection [1].

High impact information on Traf2

• Tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2) can interact with various members of the TNF receptor family [2].
• Using these double-knockout mice, we show that in the absence of TRAF2, the T helper-dependent antibody response, CD40-mediated proliferation, and NF-kappaB activation are defective [2].
• In this study, we demonstrate that TRAF2-deficient macrophages produce increased amounts of nitric oxide (NO) and TNF in response to TNF stimulation [2].
• UVB-induced association of tumor necrosis factor (TNF) receptor 1/TNF receptor-associated factor-2 mediates activation of Rel proteins [3].
• OX40-mediated memory T cell generation is TNF receptor-associated factor 2 dependent [4].

Biological context of Traf2

• CPT treatment completely abrogated the TNF-induced NF-kappa B activation, and mRNA expression of the antiapoptotic factors TNF-receptor associated factor 2, FLICE-inhibitory protein, and X-linked inhibitor of apoptosis protein was also inhibited by CPT [5].

Anatomical context of Traf2

• TRAF2 overexpression induced differentiation of osteoclast progenitors from wildtype mice into TRACP(+) multinucleate cells [1].
• The in situ localization study of proapoptosis (TRADD, caspase 3) and anti-apoptosis gene products (TRAF2) indicated that these were expressed in the basophilic cytoplasm (infected muscle cell origin) of the nurse cells [6].
• Cutting edge: profound defect in T cell responses in TNF receptor-associated factor 2 dominant negative mice [7].
• Cutting edge: molecular mechanisms of synergy between CD40 and the B cell antigen receptor: role for TNF receptor-associated factor 2 in receptor interaction [8].
• We have previously reported that TROY induces the activation of nuclear factor kappaB via TNF receptor-associated factor 2, 5, and 6, and is strongly expressed in the developing central nervous system, including the olfactory bulb [9].

Associations of Traf2 with chemical compounds

• Previously, we reported that TRAF2-deficient mice die prematurely and have elevated serum TNF levels [2].

Other interactions of Traf2

• TRAF2 is essential for TNF-alpha-induced osteoclastogenesis [1].
• TRAF2 deficiency results in hyperactivity of certain TNFR1 signals and impairment of CD40-mediated responses [2].
• These data extend the recent demonstration that TRAF2 mediated JNK activation in response to endoplasmic reticulum stress and strongly strengthened the idea that endogenous stress signals initiated in the endoplasmic reticulum proceed by a pathway similar to that initiated by plasma membrane receptors in response to extracellular signals [10].

References