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Translational Biology & Molecular Medicine

Houston, Texas

Benchtop, Research, Bedside and Application
Translational Biology & Molecular Medicine Graduate Program
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Thomas A. Cooper, M.D.

Thomas A. Cooper, M.D.

Department of Pathology and Immunology

Phone: 713-798-3141
Fax: 713-798-5838
Lab Web Site: Tom Cooper Laboratory


  • M.D., Temple University Medical School, Philadelphia, PA
  • Postdoctoral, University of California, San Francisco

Research Interests

  • Pathogenesis of myotonic dystrophy
  • Pre-mRNA splicing and human disease
  • Developmental regulation of alternative splicing
  • Mouse models

Selected Publications

  • Kalsotra A, Wang K, Li PF, Cooper TA. MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development. Genes Dev. 2010 Apr 1;24(7):653-8.
  • Cooper TA. Chemical reversal of the RNA gain of function in myotonic dystrophy. Proc Natl Acad Sci U S A. 2009. 106(44):18433-4.
  • Wang GS, Kuyumcu-Martinez MN, Sarma S, Mathur N, Wehrens XH, Cooper TA. PKC inhibition ameliorates the cardiac phenotype in a mouse model of myotonic dystrophy type 1. J Clin Invest. 2009. 119(12):3797-806.
  • Cooper TA.Molecular biology. Neutralizing toxic RNA. Science. 2009. 325(5938):272-3.
  • Cooper TA, Wan L, Dreyfuss G. RNA and disease. Cell. 2009. 136(4):777-93.
  • Kalsotra A, Xiao X, Ward AJ, Castle JC, Johnson JM, Burge CB, Cooper TA. A postnatal switch of CELF and MBNL proteins reprograms alternative splicing in the developing heart. Proc Natl Acad Sci U S A. 2008. 105(51):20333-8.
  • Orengo JP, Chambon P, Metzger D, Mosier DR, Snipes GJ, Cooper TA. Expanded CTG repeats within the DMPK 3' UTR causes severe skeletal muscle wasting in an inducible mouse model for myotonic dystrophy. Proc Natl Acad Sci U S A. 2008. 105(7):2646-51.

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