Kurt W. Prins

     Email: prin0088@umn.edu

     Year entered: 2008

     Degrees received:
     University of Wisconsin-Madison
     B.S., 2006

     University of Minnesota
     Ph.D., 2010, Biochemistry, Molecular Biology and Biophysics Graduate
     M.D., 2012, Medical School

Honors and awards:
-University of Minnesota Graduate School Fellowship, 2006-2007
-Predoctoral Fellowship from NIH Training Program in Muscle Research, 2007-2008
-Gregory Marzolf Muscular Dystrophy Fellowship, 2008-2009
-Dr. Marvin and Hadassah Bacaner Research Award 2010
-Beatrice Z. Milne and Theodore Brandenburg Award 2010
-Ross A. Gortner Award 2010
-American Association for the Advancement of Science Program for Excellence in Science 2009-2011

Thesis advisor: James Ervasti, Ph.D.

Thesis research:
Duchenne muscular dystrophy (DMD) is a lethal muscle-wasting disease affecting approximately 1 in every 3500 males.  DMD results from the loss of dystrophin, a 427 kDa protein localized to the subsarcolemmal space of muscle cells.  Dystrophin functions to link the cytoskeleton to the extracellular matrix, thereby providing structural support to muscle cell membranes.  The goal of my thesis research is to investigate how cytoskeletal components interact with dystrophin and how loss of such components affects muscle function.

Publications (pubmed):

Prins KW, Call JA, Lowe DA, Ervasti JM. Quadriceps myopathy caused by skeletal muscle specific ablation of bcyto-actin. J. Cell Sci. 2011;124:951-957.

Prins KW, Humston JL, Mehta A, Tate V, Ralston E, Ervasti JM. Dystrophin is a microtubule-associated protein. J Cell Biol. 2009;186:363-369.

Jaeger MA, Sonnemann KJ, Fitzsimons DP, Prins KW, Ervasti JM. 2009. Context-dependent functional substitution of alpha-skeletal actin by gamma-cytoplasmic actin. FASEB J. 23:2205-2214

Bunnell TM, Jaeger MA, Fitzsimons DP, Prins KW, Ervasti JM. Destabilization of the dystrophin-glycoprotein complex without functional deficits in alpha-dystrobrevin null muscle. PLoS ONE 2008;3:e2604.

Prins KW, Lowe DA, Ervasti JM. Skeletal muscle-specific ablation of gamma(cyto)-actin does not exacerbate the mdx phenotype. PLoS ONE 2008;3:e2419.