Transforming growth factor β-activated kinase 1 (TAK1 or MAP3K7) is a key signaling component of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. Activation of TAK1 is tightly regulated through its binding partners and protein modifications. Although TAK1 functions as an essential and positive regulator of innate immune signaling and apoptosis in mouse embryonic fibroblasts (MEFs), T cells, and other cells, it negatively regulates cell development and activation of proinflammatory signaling pathways in neutrophils. However, the molecular mechanisms responsible for the opposite roles of TAK1 in different cell types remain to be addressed. In this article, we discuss the latest progresses in our understanding of TAK1 regulation, function, and mechanisms in a cell-type specific manner.
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