Biochemistry & Cancer Biology

Amir Askari, Ph.D.


Professor Emeritus

Telephone: (419) 383-4131, 383-3982
FAX: (419) 383-6228


  • B.S., Biology, 1953, University of Dubuque, Dubuque, Iowa
  • M.S., Chemistry, 1956, New York University
  • Ph.D., Biochemistry, 1960, Cornell University Medical College
  • Instructor, Pharmacology, Cornell University Medical College, 1963-1964
  • Assistant Professor of Pharmacology, Cornell University Medical College, 1964-1967
  • Associate Professor of Pharmacology, Cornell University Medical College, 1967-1973
  • Acting Chairman, Pharmacology, Cornell University Medical College, 1971-1972
  • Professor of Pharmacology, Cornell University Medical College, 1973-1975
  • Professor of Physiology and Biophysics, Graduate School of Medical Sciences, Cornell University Medical College, 1973-1975
  • Professor and Chairman of Pharmacology and Therapeutics, Medical College of Ohio, 1975-1997
  • Professor of Pharmacology and Therapeutics, 1997-2005
  • Professor and Chairman, Department of Physiology and Pharmacology, University of Toledo College of Medicine, Health Science Campus, 2006-2009
  • Professor of Physiology and Pharmacology, University of Toledo College of Medicine, 2010-2011
  • Professor, Department of Biochemistry & Cancer Biology, University of Toledo College of Medicine, 2011-2015
  • Professor Emeritus, Department of Biochemistry & Cancer Biology, University of Toledo College of Medicine & Life Sciences, 2015-present
Research Interests:

The laboratory has had a long-standing interest in the mechanism of ion transport across biological membranes, with a major emphasis on the properties and functions of (Na+,K+)-ATPase (the sodium pump) of the eucaryotic plasma membrane.  Current work of the laboratory is primarily on the digitalis-induced interactions of (Na+,K+)-ATPase with non-ATPase proteins, leading to the newly discovered functions of (Na+,K+)-ATPase as a signal transducer that regulates growth of the cardiac myocyte.  Recent findings include the discovery that digitalis drugs induce cardiac hypertrophy through the activation of P13K/Akt signaling pathways, and that this drug-induced hypertrophy is akin to physiological rather than pathological cardiac hypertrophy.  We are currently testing the hypothesis that low-dose digitalis treatment prevents pressure overload-induced cardiac hypertrophy and failure.

Representative Publications

A. Askari and D. B. Melville, "The reaction sequence in ergothioneine biosynthesis."  J. Biol. Chem., 237, 1615 (1962).

A. Askari, "Erythrocytes:  5'-adenylic acid deaminase requirement for ammonia or monovalent metal ion."  Science, 141, 44 (1963).

A. Askari, "Effect of ATP and monovalent cations on brain adenylate acid deaminase."  Nature, 202, 185 (1964).

A. Askari, "Uptake of some quaternary ammonium ions by human erythrocytes."  J. Gen. Physiology, 49, 1147 (1966).

A. Askari, Editor, "Proceedings of the First International Conference on Properties and Functions of Na+,K+-ATPase."  Ann. N. Y. Acad. Sciences, 242, (1974).

A. Askari, W. Huang and J. Antieau, "Na+,K+-ATPase:  Ligand-induced conformational transitions and alterations in subunit interactions evidenced by cross-linking studies."  Biochemistry, 19, 1132 (1980).

W. Huang and A. Askari, "Simultaneous bindings of ATP and vanadate to (Na++K+)-ATPase:  Implications for the reaction mechanism of the enzyme."  J. Biol. Chem., 259 13287 (1984).

A. Askari, S. S. Kakar, and W.-H. Huang, "Ligand binding sites of the ouabain-complexed (Na+,K+)-ATPase."  J. Biol. Chem., 263, 235-242 (1988).

M.G. Jack, W.-H. Huang, and A. Askari, "Characterization of Na+-dependent phosphate transport in cardiac sarcolemmal vesicles."  J. Biol. Chem., 264, 3904-3908 (1989).

M. Ganjeizadeh, N. Zolotarjova, W.-H. Huang, and A. Askari, "Interactions of phosphorylation and dimerizing domains of the a-subunits of Na+/K+-ATPase".  J. Biol. Chem. 270, 15707-15710 (1995).

M. Peng, L. Huang, Z. Xie, W.-H. Huang, and A. Askari, "Partial inhibition of Na+/K+-ATPase by ouabain induces the Ca2+-dependent expressions of early-response genes in cardiac myocytes".  J. Biol. Chem. 271, 10372-10378 (1996).

 Z. Xie and A. Askari.  “Na+/K+-ATPase as a Signal Transducer”.  Eur. J. Biochem. 269, 2434-2439 (2002).

P. Kometiani, L. Liu, and A. Askari.  “Digitalis-Induced Signaling by Na+/K+-ATPase In Human Breast Cancer Cells”.  Mol. Pharmacol. 67, 929-936 (2005).

L. Liu and A. Askari.  “The Beta-Subunit of Cardiac Na+/K+-ATPase Dictates the Concentration of the Functional Enzyme in Caveolae”.  Am. J. Physiol. Cell. Physiol. 291, C569-C578 (2006).

L. Liu, X. Zhao, S.V. Pierre, and A. Askari.  “Association of PI3K/Akt Signaling Pathway with Digitalis-Induced Hypertrophy of Cardiac Myocytes”.  Am. J. Physiol. Cell Physiol. 293, C1489-C1497 (2007).

G.A. Morrill, A.B. Kostellow, and A. Askari.  “Progesterone Modulation of Transmembrane Helix-Helix Interactions Between the Alpha-Subunit of Na/K-ATPase and Phospholipid N-Methyltransferase in the Oocyte Plasma Membrane”.  BMC Struct. Biol. 25: 10-12 (2010).

Liu, L., A.V., Ivanov, M.E. Gable, F. Jolivel, G.A. Morrill, and A. Askari.  “Comparative properties of caveolar and noncaveolar preparations of kidney Na+/K+-ATPase.  Biochemistry 50: 8664-8673 (2011). 

Y. Bai, E.E. Morgan, D.R. Giovannucci, S.V. Pierre, K.D. Philipson, A. Askari, and L. Liu.  “Different roles of the cardiac Na+/Ca2+-exchanger in ouabain-induced inotropy, cell signaling, and hypertrophy.  Am. J. Physiol. Heart Circ. Physiol. 304: H427-H435 (2012).

J. Wu, E.E. Akkuratov, Y. Bai, C.M. Gaskill, A. Askari, and L. Liu.  “Cell signaling associated with Na(+)/K(+)-ATPase: activation of phosphatidylinositide 3-kinase IA/Akt by ouabain is independent of Src.  Biochemistry 52: 9059-9067 (2013). 

M.E. Gable, S.L. Abdallah, S.M. Najjar, L. Liu and A. Askari.  Digitalis-induced cell signaling by the sodium pump: On the relation of Src to Na(+)/K(+)-ATPase.  Biochem. Biophys. Res. Commun. 446: 1151-1154 (2014).

Last Updated: 6/26/15