Recombinant Human TRAF2

Background

TRAF2 is a key adaptor protein that links TNF receptors and other immune receptors to downstream signaling pathways, particularly NF-κB and JNK activation, to regulate inflammation, cell survival, and apoptosis. TRAF2 interacts with TNFR1, TNFR2, and CD40 to recruit signaling intermediates like RIPK1 and IKK, facilitating the activation of NF-κB-dependent transcription of pro-survival and pro-inflammatory genes. It plays a critical role in immune homeostasis and inflammation, particularly in T cells, B cells, and macrophages. TRAF2 also regulates apoptosis by inhibiting caspase-8 activation through recruitment of cIAP proteins. Dysregulation of TRAF2 is implicated in autoimmune diseases, chronic inflammatory conditions, and cancers, where excessive or impaired NF-κB signaling contributes to disease pathogenesis. Knockout studies reveal embryonic lethality, defective TNF-induced NF-κB activation, and increased apoptosis, highlighting its essential role in maintaining cell survival and immune responses.