Gab2 and Gab3 Redundantly Suppress Colitis by Modulating Macrophage and CD8 T-Cell Activation.

Inflammatory Bowel Disease (IBD) is a multi-factorial chronic inflammation of the gastrointestinal tract prognostically linked to CD8 T-cells, but little is known about their mechanism of activation during initiation of colitis. Here, Grb2-associated binding 2/3 adaptor protein double knockout mice (Gab2/3) were generated. Gab2/3 mice, but not single knockout mice, developed spontaneous colitis.

Grb2-associated binding (Gab) proteins in hematopoietic and immune cell biology.

Grb2-associated binding (Gab) scaffolding/adapter proteins are a family of three members including mammalian Gab1, Gab2, and Gab3 that are highly conserved. Since the discovery of these proteins, there has been an extensive amount of work done to better understand Gab functional roles in multiple signaling pathways, typically acting as a downstream effectors of receptor-tyrosine kinase (RTK)-triggered signal transduction. In addition to their participation in hematopoiesis, Gabs play important roles in regulation of immune response and in also in cancer cell signaling.