Invitrogen™ Human MADD Synthetic Peptide

Tumor necrosis factor receptor 1 (TNFR1) contains a death receptor domain that mediates interactions involved in downstream signaling of TNF. A novel protein, MADD (mitogen activated protein (MAP)-kinase activating death domain protein) has recently been shown to associate with the death domain of TNFR1 through its own C-terminal death domain. This interaction is critical for TNFR1 signal generation. Overexpression of MADD activates the MAP (Mitogen Activated Protein) kinases extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) and induces the phosphorylation of cytosolic phospholipase A2. This discovery suggests that MADD links tumor necrosis factor TNF and MAP kinase activation and arachidonic acid release. MADD has a 98% homology with another protein, differentially expressed in neoplasmic vs. normal cells (DENN). DENN is a substrate for JNK3, and is important in the hypoxia and stress induced intracellular signalling pathways. MADD also has a 93% sequence conservation with a GDP/GTP exchange protein, Rab3.