James Alb, Ph.D.


Assistant Professor

  • B.S., Purdue University Calumet, 1990
  • M.S., University of Illinois, 1992
  • Ph.D., University of Alabama at Birmingham, 1997

Research Interests

We utilize gene knockout technology in both cells and mice to study a class of proteins called phosphatidylinositol transfer proteins (PITPs). These proteins are thought to play key roles in lipid signaling events in the nucleus, Golgi, and cell surface. The knockout experiments we have performed to date have led to a new understanding of the roles these proteins play both cellularly and in whole animal studies. The consequences of losing function of one isoform (PITPa) of this family is very dramatic in the mouse which is characterized by neurodegeneration and a fatal intestinal fat absorption defect closely mimicking human chylomicron retention disease. We have also generated a knockout mouse line for another isoform in this family (PITPb) and have found this to be an early embryonic lethal event; suggesting an important, previously unidentified, developmental role for this gene.

Selected Publications

PubMed 1

  • Alb, JG Jr, Phillips SE, Wilfley LR, Philpot BD, Bankaitis VA. 2007. The pathologies associated with functional titration of phosphatidylinositol transfer protein alpha activity in mice. J Lipid Res. 48:1857-72.
  • Morin-Kensicki EM, Boone BN, Howell M, Stonebraker JR, Teed J, Alb JG, Magnuson TR, O'Neal W, Milgram SL. 2006. Defects in yolk sac vasculogenesis, chorioallantoic fusion, and embryonic axis elongation in mice with targeted disruption of Yap65. Mol Cell Biol. 2006. 26: 77-87.
  • Alb JG Jr, Cortese JD, Phillips SE, Albin RL, Nagy TR, Hamilton BA, Bankaitis VA. 2003. Mice lacking phosphatidylinositol transfer protein alpha exhibit spinocerebellar degeneration, intestinal and hepatic steatosis, and hypoglycemia. J. Biol. Chem. 278: 33501-33518.
  • Alb, Jr., J., Phillips, S, Rostand, K., Xiaxia, C., Pinxteren J., Cotlin, L., Manning, T., Gua, X., York, J., Sontheimer, H., Collawn, J., and Bankaitis, V. Genetic Ablation of Phosphatidylinositol Transfer Protein Function in Murine Embryonic Stem Cells. Mol Biol. Cell 2002. 13: 739-734.
  • Nemoto, Y., Kearns, b., Wenk, M., Chen, H., Mori, K., Alb, Jr., J., and De Camilli, P. Functional Characterization of a Mammalian Sac1 and Mutants Exhibiting Substrate-Specific Defects in Phosphoinositide Phosphatase Activity. Jour. Biol. Chem. 2000. 275 (44): 34293-305.
  • Alb, Jr., J., Kearns, M, and Bankaitis, V. Phospholipid Metabolism and Membrane Dynamics. Current Opinion in Cell Biology. 1996. 8: 534-541.
  • Alb, Jr., J., Gedvilaite, A., Cartee, R., Skinner, H., and Bankaitis, V. Mutant Rat Phosphatidylinositol/Phosphatidylcholine Transfer Protein Specifically Defective in Phosphatidylinositol Transfer: Implications fro the Regulation of Phospholipid Transfer Activity. Pro. Natl. Acad. Sci. 1995. 92: 8826-8830.