Michael Sinensky

Michael Sinensky

Adjunct Professor and Lecturer

Professor Emeritus, J. H. Quillen College of Medicine, East Tennessee State University
DH 602
(408) 924-5504
michael.sinensky@sjsu.edu

Education

B.A. Chemistry 1966, Columbia College
Ph.D. Biochemistry and Molecular Biology 1972, Harvard University

Courses Taught

Biochemistry

Research Interests

  • The role of mevalonate metabolism in mammalian cell-cycle progression. Structure and function of prenylated proteins. Of particular current interest is the role of prenylation dependent processing of the nuclear lamina proteins in regulation of cell growth, metabolism and signaling.
  • Genetic and metabolic regulation of biosynthetic enzymes in mammalian cells utilizing isoprenoid biosynthesis as a model system.
  • The structure-function relationships of membrane lipids, the mechanism of regulation of membrane lipid composition and the role of structural parameters of cell membrane lipids in regulation of their biosynthesis.
  • The signal transduction pathway of oxysterol induced apoptosis.

Selected Publications

  • Liu J, Netherland C, Pickle T, Sinensky MS, Thewke DP. Stimulation of Akt poly-ubiquitination and proteasomal degradation in P388D1 cells by 7-ketocholesterol and 25-hydroxycholesterol. Arch Biochem Biophys. Arch Biochem Biophys. 487:54-8 ( 2009).
  • Liu Y, Wang Y, Rusinol AE, Sinensky MS, Liu J, Shell SM, Zou Y.Involvement of xeroderma pigmentosum group A (XPA) in progeria arising from defective maturation of prelamin A.FASEB J. 22:603-11 ( 2008)
  • Dechat T, Shimi T, Adam SA, Rusinol AE, Andres DA, Spielmann HP, Sinensky MS, Goldman RD. Alterations in mitosis and cell cycle progression caused by a mutant lamin A known to accelerate human aging. Proc Natl Acad Sci U S A. 104:4955-60 ( 2007).
  • Rusiñol AE, Sinensky MS. Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors.J Cell Sci. 119: 3265-72 ( 2006).
  • Liu Y, Rusinol A, Sinensky M, Wang Y, Zou Y. DNA damage responses in progeroid syndromes arise from defective maturation of prelamin A. J Cell Sci. 119:4644-9 ( 2006)