Abstract

Tumor necrosis factor (TNF) causes activation of the transcription factor NF-κB by activating TNF receptors on the cell surface. The receptor then binds TRAF adaptor proteins, which couple it to a series of kinases that ultimately lead to control of NF-κB. A new family of protein kinases that are related to the I-κB kinases has now been identified that may couple TRAF2 to transcriptional activation. Although its characterization has so far only been accomplished in transiently transfected cells, TBK1 (for TANK-binding kinase 1) appears to function in a complex with TRAF2 and TANK, a TRAF-binding protein. Physiological substrates for TBK1 are not yet known, but it appears to represent another important component in the complex regulation of NF-κB.Pomerantz, J.L., and Baltimore, D. (1999) NF-κB activation by a signaling complex containing TRAF2, TANK, and TBK1, a novel IKK-related kinase. EMBO J. 18: 6694-6704. [Abstract] [Full Text]

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