The NF-k B transcription factor coordinates a response to pathogens and pro-inflammatory cytokines, and is vital in the development of acute and chronic inflammatory diseases. NF-k B is activated by cytokine-activated IKB kinases (IKKs) found in large complexes. The IKK complexes consist of NIK, IKK-a, IKK-b , IkB-a, NF-k B/RelA and IKK-complex-associated protein (IKAP). First identified as a scaffolding protein of the IKK complex, IKAP, also known as elongation protein 1 (ELP1), has been linked to adhesion and migration in several cell types, including rat primary neurons. Depletion of IKAP by loss-of-function mutations in the IKBKAP gene has been shown to cause defective neuronal development and maintenance, leading to familial dysautonomia (FD). FD is a hereditary neuronal disease characterized by poor development and progressive degeneration of the sensory and autonomic nervous system. In addition, IKAP associates with c-Jun N-terminal kinase (JNK) and could specifically enhance JNK activation induced by the upstream JNK activators MEKK1 and ASK1, indicating another possible cause for FD.
Naumanen, T. et al. (2008) Cel. Adh. Migr. 2(4):236.
Cohen, L. et al. (1998) Nature 395:292.
*For more information, see UniProt Accession O95163
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*All molecular weights (MW) are confirmed by comparison to Bio-Rad Rainbow Markers and to western blot mobilities of known proteins with similar MW.
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