TAB1

TAB1, short for TAK1-binding protein 1, is a protein encoded by the human TAB1 gene (also known as MAP3K7IP1). It functions as an adaptor and regulator in the TAK1 signaling pathway, rather than as an enzyme. TAB1 participates in forming a signaling complex with TAK1 (MAP3K7) and, together with related adaptors TAB2 and TAB3, helps enable TAK1 activation in response to various stimuli.

In response to inflammatory and stress signals, including cytokines such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) as well as transforming growth factor family members, the TAB1-containing complex activates TAK1. Activated TAK1 then triggers downstream pathways, notably the NF-κB and JNK/p38 MAP kinase cascades, which regulate inflammatory gene expression, cell survival, and stress responses.

Molecularly, TAB1 is a cytoplasmic protein characterized by regions that promote protein–protein interactions, particularly coiled-coil motifs. It functions as a scaffold rather than possessing catalytic activity. Its activity can be modulated by phosphorylation and other post-translational modifications, and TAB1 is expressed across a wide range of human tissues.

Clinical and research notes indicate that TAB1 plays a significant role in proper TAK1 activation and signaling. Dysregulation of TAB1–TAK1 signaling has been investigated in the context of inflammatory diseases and cancer in various models. As a key component of the TAK1 signaling axis, TAB1 remains a focus of studies aimed at modulating NF-κB and MAPK–mediated responses.

Related proteins include TAB2 and TAB3, which can form alternative TAK1-activating complexes with MAP3K7.