Robert J. Kelm, Jr., PhD

Education:

Graduate School
University of Vermont
College of Medicine
Department of Biochemistry

Training:

Residency

Fellowship

Mayo Clinic/Foundation
Department of Biochemistry and Molecular Biology
Rochester, MN 55905

Specialty:

Cardiovascular Biology & Disease
Regulation of Gene Expression
Protein-Nucleic Acid Interactions

Certifications:

Academic Appointments:

Biography:

Dr. Kelm received his Ph.D. in Biochemistry from the University of Vermont College of Medicine in 1991. Upon completion of his Ph.D. studies, he joined Haematologic Technologies, Inc. as a Scientist and was later appointed Director of Assay Development. Dr. Kelm returned to academia in late 1994 as a Research Fellow in the Department of Biochemistry and Molecular Biology at the Mayo Clinic to pursue research involving single-stranded DNA/mRNA-binding proteins. In October, 2001, Dr. Kelm joined the UVM faculty as an Assistant Professor in the Department of Medicine. In January, 2002, he was appointed as an adjunct Assistant Professor in the Department of Biochemistry. Dr. Kelm was promoted to Associate Professor with tenure in July, 2006.

Major Research Interests:

The primary focus of Dr. Kelm’s research program is the study of gene regulatory mechanisms and transcription factors responsible for promoting phenotypic changes in cardiovascular cell types during development and in disease. He is particularly interested in understanding how smooth muscle cells and fibroblasts trans-differentiate in response to environmental signals promoting wound repair and vascular remodeling.

Arteriosclerosis (arterial wall thickening) is a progressive tissue remodeling process that is caused by chronic inflammatory disease and acute vascular injury. Restriction of blood flow due to luminal expansion of the vessel wall can lead to lethal outcomes such as heart attack or stroke. Importantly, down-regulation of contractile protein expression in stromal fibroblasts and vascular smooth muscle cells is associated with a switch to a fibroproliferative phenotype and may be critical in progression of disease. Delineation of the mechanism(s) operating in these cell types is a focus of the work. Identification has been accomplished of several novel single-stranded DNA (ssDNA)/mRNA-binding proteins that possess the capacity to alter SMaA expression at the level of transcription and translation. He is testing effects on SMaA gene repression by certain members of the Pur and Y-box families of ssDNA/RNA proteins. Experiments are designed to acquire both qualitative and quantitative information about the physical and functional properties of Pura, Purb, and MSY1 in the test tube and in specific cell types. He is also pursuing studies in vivo to elucidate physiological roles of these proteins in vascular disease and injury.

Publications:

Representative Publications from a total of 30

Wang, S. X., Elder, P. K., Zheng, Y., Strauch, A. R., and Kelm, R. J., Jr. (2005) Cell cycle-mediated regulation of smooth muscle a-actin gene transcription in fibroblasts and vascular smooth muscle cells involves multiple adenovirus E1A-interacting cofactors. J. Biol. Chem. 280:6204-6214

Knapp, A. M., Ramsey, J. E., Wang, S. X., Godburn, K. E., Strauch, A. R., and Kelm, R. J., Jr. (2006) Nucleoprotein interactions governing cell type-specific repression of the mouse smooth muscle a-actin promoter by single-stranded DNA-binding proteins Pura and Purb. J. Biol. Chem. 281:7907-7918

Ramsey, J. E., Daugherty, M. A., and Kelm, R. J., Jr. (2007) Hydrodynamic studies on the quaternary structure of recombinant mouse Purb . J. Biol. Chem. 282:1552-1560