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Background
A structurally diverse repertoire of ligands, from photons to large peptides, activates GPCRs to elicit their physiological functions. Ligand-bound GPCRs, in turn, function as guanine nucleotide exchange factors catalyzing the exchange of GDP bound on the Gα subunit with GTP in the presence of Gβγ, causing the dissociation of the Gα subunit from the Gβγ dime to form two functional units (Gα and Gβγ). Both Gα and Gβγ subunits signal to various cellular signaling pathways. Based on the sequence and functional homologies, G proteins are grouped into four families: Gs, Gi, GGq, and G12. As increasing numbers of effectors and interacting proteins for these G proteins have been identified, the physiological processes in which G proteins participate are multiplying.

Among the four subfamilies of G proteins, the function of G12/13 subfamily is less well understood. In this family, there are two members, G12 and G13, that are expressed ubiquitously. Gα12 knockout mice appeared normal. Gα13 knockout mice displayed embryonic lethality (~E9.5). The Gα13-/- mouse embryos had defective vascular systems. G13 is also essential for receptor tyrosine kinase-induced migration of fibroblast and endothelial cells.

Assay Principle
The Gα13 Activation Assay Kit uses configuration-specific anti-Gα13-GTP Mouse monoclonal antibody to measure Gα13-GTP levels in cell extracts or in vitro GTPγS loading Gα13 activation assays. Anti-Gα13-GTP mouse monoclonal antibody is first incubated with cell lysates containing Gα13-GTP. Next, the GTP-bound Gα13 is pulled down by protein A/G agarose. Finally, the precipitated Gα13-GTP is detected through immunoblot analysis using anti-Gα13 mouse monoclonal antibody.