Biosciences Graduate Program

Eric B. Taylor, PhD


Assistant Professor of Biochemistry

Contact Information

Office: 3316 PBDB
Iowa City, IA 52242
Office Phone: 319-384-4098

Web: Taylor Laboratory
Web: Google Scholar Citations


BS, Exercise Physiology, Brigham Young University
PhD, Physiology, Brigham Young University

Post Doctoral, Joslin Diabetes Center and Harvard Medical School
Post Doctoral, University of Utah School of Medicine

Education/Training Program Affiliations

Biosciences Graduate Program
Department of Biochemistry PhD
Interdisciplinary Graduate Program in Molecular and Cellular Biology
Medical Scientist Training Program

Research Summary

Mitochondria are the engine of eukaryotic cellular metabolism. Mitochondria sustain cells with a continuous supply of ATP, replenish metabolic intermediates, and coordinate metabolic flux with numerous aspects of cellular biology. Accordingly, mitochondrial dysfunction is a root cause of devastating diseases, including cancer, neurodegeneration, and diabetes. The Taylor Lab is interested in the molecular mechanisms regulating mitochondrial function and their relationship to disease. Our research program is multidisciplinary, utilizing genetic, biochemical, cellular, and physiological experimental approaches. We have additional interest in problems related to skeletal muscle function and diabetes. Our current research projects focus on novel proteins important for mitochondrial function. The first is on VMS1, a protein that recruits components of the ubiquitin proteasome system to stressed mitochondria to extract damaged proteins for presentation to the proteasome, thereby maintaining mitochondrial protein quality. Thus, VMS1 may be relevant to any disease involving progressive mitochondrial failure. The second is on the mitochondrial pyruvate carrier (MPC), which Dr. Taylor recently co-discovered. Mitochondrial pyruvate uptake is critical for ATP production by the TCA cycle and for generating the synthetic intermediates supporting fat, protein, and carbohydrate metabolism. Therefore, MPC function is essential for normal physiology and its disruption causes diverse and severe metabolic abnormalities. We are interested in discovering the mechanisms regulating the function of the MPC molecule.

Center, Program and Institute Affiliations

Cardiovascular Research Center
Fraternal Order of Eagles Diabetes Research Center
Holden Comprehensive Cancer Center
Obesity Initiative

Selected Publications

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Bricker D, Taylor E, Schell J, Orsak T, Boutron A, Chen Y, Cox J, Cardon C, Van Vranken J, Dephoure N, Redin C, Boudina S, Gygi S, Brivet M, Thummel C, Rutter J.  A mitochondrial pyruvate carrier required for pyruvate uptake in yeast, Drosophila, and humans.  Science (New York, N.Y.).  2012 July. 337(6090):96-100.

Chen Y, Taylor E, Dephoure N, Heo J, Tonhato A, Papandreou I, Nath N, Denko N, Gygi S, Rutter J.  Identification of a protein mediating respiratory supercomplex stability.  Cell metabolism.  2012 March. 15(3):348-60.

Taylor E, Rutter J.  Mitochondrial quality control by the ubiquitin-proteasome system.  Biochemical Society transactions.  2011 October. 39(5):1509-13.

Heo J, Livnat-Levanon N, Taylor E, Jones K, Dephoure N, Ring J, Xie J, Brodsky J, Madeo F, Gygi S, Ashrafi K, Glickman M, Rutter J.  A stress-responsive system for mitochondrial protein degradation.  Molecular cell.  2010 November. 40(3):465-80.

Treebak J, Taylor E, Witczak C, An D, Toyoda T, Koh H, Xie J, Feener E, Wojtaszewski J, Hirshman M, Goodyear L.  Identification of a novel phosphorylation site on TBC1D4 regulated by AMP-activated protein kinase in skeletal muscle.  American journal of physiology. Cell physiology.  2010 February. 298(2):C377-85.

Taylor E, An D, Kramer H, Yu H, Fujii N, Roeckl K, Bowles N, Hirshman M, Xie J, Feener E, Goodyear L.  Discovery of TBC1D1 as an insulin-, AICAR-, and contraction-stimulated signaling nexus in mouse skeletal muscle.  The Journal of biological chemistry.  2008 April. 283(15):9787-96.

Kramer H, Taylor E, Witczak C, Fujii N, Hirshman M, Goodyear L.  Calmodulin-binding domain of AS160 regulates contraction- but not insulin-stimulated glucose uptake in skeletal muscle.  Diabetes.  2007 December. 56(12):2854-62.

Taylor E, Goodyear L.  Targeting skeletal muscle AMP-activated protein kinase to treat type 2 diabetes.  Current diabetes reports.  2007 December. 7(6):399-401.

Taylor E, Lamb J, Hurst R, Chesser D, Ellingson W, Greenwood L, Porter B, Herway S, Winder W.  Endurance training increases skeletal muscle LKB1 and PGC-1alpha protein abundance: effects of time and intensity.  American journal of physiology. Endocrinology and metabolism.  2005 December. 289(6):E960-8.

Taylor E, Ellingson W, Lamb J, Chesser D, Winder W.  Long-chain acyl-CoA esters inhibit phosphorylation of AMP-activated protein kinase at threonine-172 by LKB1/STRAD/MO25.  American journal of physiology. Endocrinology and metabolism.  2005 June. 288(6):E1055-61.

Date Last Modified: 07/30/2014 - 12:56:18