The Git version control system lets you create and manage repositories (called a "repo") for your projects, and use common Git commands. This resource will help you get started with Git by walking through the creation of a repository, basic file management and how to commit changes. This tutorial also introduces partial bundles, a new way to package up and transfer your repository.
GIT2 is a small, cell surface-associated protein that is involved in clathrin-coated pit formation and signaling. Although human GIT1 and rat GIT2 share similar catalytic activity and binding to Arf family members, they exhibit distinct cellular localizations and biological functions because of tissue-specific alternative splicing (1,2). In the hematopoietic system, GIT2 binds paxillin or PIX in focal adhesions and promotes cell migration and proliferation (3,4). The binding is regulated by phosphorylation on one or more of the five alternative tyrosine residues located within its carboxyl-terminal domain by kinases such as FAK and Src (5,6). Inhibition of tyrosine phosphorylation reduces the association of GIT2 with paxillin or PIX and increases membrane ruffling and clathrin-coated pit turnover in HeLa cells (6,7). These effects of GIT2 are mediated by a direct interaction with Crk, which is required for activation of the actin cytoskeleton (7,8). A similar role for GIT2 is elicited in HeLa cells when its expression is reduced by lentiviral-mediated shRNA. The effects of GIT2 knockdown are reversed by expressing a recombinant GIT2 cDNA in which the target sequence has been removed by silent mutagenesis (9). GIT2 deletion disrupts insulin secretion in pancreatic islets and causes diabetic-state symptoms in mice, including elevated plasma glucose, insulin resistance and hypothalamic hyperglycemia (9).