Konstantin V. Kandror
Professor of Biochemistry
Department of Biochemistry
Boston University School of Medicine
Silvio Conte Building, K124
72 E. Concord Street
Boston, MA 02118
Phone: 617-638-5049
Fax: 617-638-5339
Email: kandror@biochem.bumc.bu.edu
Education
B.S., M.S., Moscow State University, Moscow, Russia
Ph.D., Bakh Institute of Biochemistry, Moscow, Russia
Research Interest
Diabetes mellitus represents one of the major health threats to modern civilization, and its worldwide prevalence is increasing at an alarming rate. In diabetes, insulin cannot stimulate glucose entry into the cell, as it does in normal individuals. As a result, extra glucose stays in the blood and causes multiple health problems. As insulin-regulated glucose transport is the major molecular defect in diabetes, it represents the main focus of our lab. Insulin activates glucose uptake by translocating glucose transporter isoform 4 (Glut4) from its intracellular vesicular storage pool to the plasma membrane. This process, along with exocytosis of synaptic vesicles in neurons, insulin-containing granules in the pancreas, water channel-containing vesicles in the kidney, etc., represents an example of a widely spread type of the biological regulation via regulated exocytosis. Impaired translocation of Glut4-containing vesicles in diabetes may have two explanations. First, the molecular defect may lie in the signal transduction pathway that connects the insulin receptor in the plasma membrane and intracellular Glut4-vesicles. Second, the cell biology (i.e. the protein composition, biogenesis, intracellular trafficking) of Glut4-vesicles may be impaired. Our lab pursues both these directions using the wide arsenal of modern techniques that include molecular biological methods, protein biochemistry, subcellular fractionation, microscopy and in vivo studies.
Recent Publications
- Belfort G.M., K. Bakirtzi and K.V. Kandror. Cellugyrin Induces Biogenesis of Synaptic-Like Micro-Vesicles in PC12 Cells. J. Biol. Chem., 2005, 280, 7262-7272.
- Shi, J. and Kandror, K.V. Sortilin is essential and sufficient for the formation of Glut4 storage vesicles. Developmental Cell, 2005, 9, 99-108.
- Tzatsos, A. and Kandror, K.V. Nutrients suppress phosphatidylinositol 3-kinase/Akt signaling via raptor-dependent mTOR-mediated insulin receptor substrate-1 phosphorylation. Mol.Cell.Biol., 2006, v. 26, 63-76.
- Shi, J. and Kandror K.V. The luminal Vps10p domain of sortilin plays the predominant role in targeting to insulin-responsive Glut4-containing vesicles”, J.Biol.Chem., 2007, v.282, 9008-9016.
