Rab 27b Background Information
The Rab family of low molecular weight GTPases are critical regulators of vesicular transport (1). Rab proteins cycle between an active GTP-bound state, which recruits specific effector proteins, and an inactive GDP-bound state (1). Two members of this family, Rab27a and Rab27b, have overlapping functions, but differ in tissue specificity (2,3). Rab27a is widely expressed with significant expression in pancreatic islets and pituitary tissue, and low expression in brain (3). Rab27b is also expressed in pituitary tissue, but is more significantly expressed in brain and spleen (3). Rab27a regulates diverse processes involving lysosome-related organelles, including melanosome motility in melanocytes and lytic granule release in cytotoxic T lymphocytes (4). Mutations in the Rab27a gene result in Griscelli syndrome (GS) or the corresponding mouse model ashen, a rare autosomal recessive disorder characterized by hypopigmentation, prolonged bleeding times, and platelet storage pool deficiency (2,4). In GS, Rab27a is not available to mediate the recruitment of melanosomes via the actin motor, myosin Va (5,6). The human Rab27b gene maps to chromosome 18q21.1, and encodes a protein that is involved in pituitary hormone secretion (3,7). Rab27b may be functionally redundant to Rab27a, as it can rescue Rab27a mutants (2).
