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Peter J Koch, Ph.D.


Dr. Peter Koch

Professor

Department of Dermatology

Center for Regenerative Medicine and Stem Cell Biology

Phone: (303) 724-0051

Fax: (303) 724-3051

E-Mail: Peter.Koch@ucdenver.edu

Director: Transgenic and Gene Targeting Core

Director: Induced Pluripotent Stem Cell Core 

Link to Dr. Koch’s Stem Cell web page

 

Affiliations and Memberships:

Department of Cell and Developmental Biology

Cancer Cell Biology Program, UC Cancer Center

Member of the Following University of Colorado Graduate School Programs:

Graduate Program in Cell Biology, Stem Cells and Development

Biomedical Sciences Program

Medical Scientist Training Program 

Education:

 

 MS

University of Heidelberg, Germany

 Ph.D.

University of Heidelberg

 Postdoctoral Fellowships

German Cancer Research Center, Heidelberg

 

National Cancer Institute/ National Institutes of Health,

Bethesda, MD

 

University of Pennsylvania, Philadelphia, PA

Previous Faculty Appointments: Baylor College of Medicine, Houston, TX

Research Interests :

Cell Adhesion Proteins, Cytoskeleton, Epithelial Cell Biology, Mouse Embryonic Development, Skin and Skin Appendage Development, Desmosomes, Blistering Skin Diseases, Skin Cancer, Cadherins, Desmogleins, Desmocollins, Plakophilins, Mouse Models of Human Diseases

Overview of Ongoing Research:

Desmosomes are multi-protein complexes which anchor the intermediate filament cytoskeleton at the plasma membrane of epithelial cells. Desmosomes also function as cell adhesion structures (cell junctions) that connect neighboring cells. Consequently, impaired desmosome function can lead to tissue fragility disorders. The classic examples of desmosomal diseases are blistering skin disorders (e.g. pemphigus diseases). In recent years, it has been shown that abnormal desmosome function can lead to severe heart diseases.

The goal of our laboratory is to elucidate the role of desmosomal genes and proteins in the normal development of the skin and its appendages (hair follicles, mammary glands). Furthermore, we are investigating how mutations in desmosomal genes lead to diseases (skin fragility disorders, skin cancer). To accomplish these goals, we are generating and characterizing genetically engineered mice which either lack expression of certain desmosomal genes (knockout mice) or which express mutant versions of these genes (transgenic mice, knockin mice). In order to understand how desmosomal genes are regulated during embryonic development of the skin and its appendages, we are also analyzing the role of epidermal signal transduction pathways (e.g. Wnt and NFкB) in regulating the expression of the desmosomal genes.

Selected Publications: 

 

Chen, J, Den, Z, Koch PJ. 2008. Loss of desmocollin 3 in mice leads to epidermal blistering. J Cell Sci. 121:2844-2849.

Schmidt A, Koch PJ. Desmosomes: Just cell adhesion or is there more? Cell Adhesion & Migration 2007;1:28-32.

Chen J, Cheng X, Merched-Sauvage M, Caulin C, Roop DR, Koch PJ. An unexpected role for keratin 10 end domains in susceptibility to skin cancer. J Cell Sci 2006 ;119:5067-76.

Den Z, Cheng X, Merched-Sauvage M, Koch PJ. Desmocollin 3 is required for pre-implantation development of the mouse embryo. J Cell Sci 2006; 119:482-9.

Cheng X, Den Z, Koch PJ. Desmosomal cell adhesion in mammalian development. Eur J Cell Biol 2005;84:215-23.

Cheng X, Koch PJ. In vivo function of desmosomes. J Dermatol 2004; 31:171-87.

Cheng X, Mihindukulasuriya K, Den Z, Kowalczyk AP, Calkins CC, Ishiko A, et al. Assessment of splice variant-specific functions of desmocollin 1 in the skin. Mol Cell Biol 2004; 24:154-63.

Koch PJ, Roop DR. The role of keratins in epidermal development and homeostasis--going beyond the obvious. J Invest Dermatol 2004;123:x-xi.

Koch PJ, de Viragh PA, Scharer E, Bundman D, Longley MA, Bickenbach J, et al. Lessons from loricrin-deficient mice. Compensatory mechanisms maintaining skin barrier function in the absence of a major cornified envelope protein. J Cell Biol 2000;151:389-400.

Koch PJ, Mahoney MG, Ishikawa H, Pulkkinen L, Uitto J, Shultz L, et al. Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3) gene in mice causes loss of keratinocyte cell adhesion with a phenotype similar to pemphigus vulgaris. J Cell Biol 1997; 137(5):1091-102.

 

Link to Other Selected Publications