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Carl A. Pinkert, PhD

Dr. Pinkert currently serves as Associate Vice President for Research with an academic appointment in the Department of Pathobiology. He joined the Auburn University College of Veterinary Medicine in 2006 as Associate Dean for Research and Graduate Studies, and Professor of Pathobiology. He previously served at the University of Rochester Medical Center as Professor of Pathology and Laboratory Medicine in the Center for Aging and Developmental Biology and as Director of the University’s Transgenics Program. Prior, at the University of Alabama at Birmingham, he was an Associate Professor of Comparative Medicine and Director of the UAB Transgenic Animal/Embryonic Stem Cell Resource and the national NIH Transgenic Mouse Development Facility.

He earned his Ph.D. in 1983 from the University of Georgia in animal reproductive physiology and was a postdoctoral fellow at the University of Pennsylvania through 1986 where he began studies related to gene expression in transgenic animals. He was a Sigma Xi national lecturer from 1993-1995, and a recipient of the 1997 Doerenkamp-Zbinden Foundation Research Prize – awarded for biomedical research that impacts on the welfare and well-being of animals used in research.

334-844-4784
cap@auburn.edu

Research Interests

Using transgenic animal modeling, Dr. Pinkert's work has illustrated the potential of modifying the immune system, enhancing growth performance and the feasibility of biopharmaceutical production ('molecular pharming'). Enabling technologies and procedures have also been developed for the genetic engineering of both nuclear and mitochondrial genes. Most recently, his laboratory has embarked on pioneering studies revolving around mitochondrial transfer techniques and the development of transmitochondrial animals.

In vertebrates, mitochondrial DNA (mtDNA) encodes 37 genes that are highly conserved across all species. In humans, mutations arising exclusively within the mitochondrial genome give rise to a class of severely debilitating and lethal disorders. Such mutations, many of which exist in a heteroplasmic state (where both normal and mutant mitochondrial genomes coexist in varying proportions), mainly affect tissues with high cellular energy requirements (e.g., brain, muscle, heart, kidney and endocrine organs).  In contrast to nuclear genes, mitochondrial gene replication and function differ markedly - from exclusive matrilineal inheritance to the presence of hundreds or thousands of mitochondria within a given cell. Various human diseases have been associated with specific mtDNA mutations including diabetes mellitus, myocardiopathy and retinitis pigmentosa, as well as age-associated changes in the functional integrity of mitochondria as seen in Parkinson's, Alzheimer's and Huntington's diseases.  Accordingly, the ability to manipulate and regulate the expression of mitochondrial genes provides a basis for developing innovative gene therapy paradigms.  In collaborative studies, the creation of transmitochondrial mice (mice harboring introduced and species-specific mitochondrial genes) represents an initial step toward providing a greater understanding of mitochondrial dynamics while paving the way for therapeutic interventions in humans and manipulation of mitochondrial genetics in a host of species.

Selected Publications

Irwin, M.H., V. Parrino and C.A. Pinkert. 2001. Construction of a mutated mtDNA genome and transfection into isolated mitochondria by electroporation. Adv. Reprod. 5:59-66.

Pinkert, C.A. Transgenic Animal Technology: A Laboratory Handbook. 2nd ed., Academic Press, Inc., San Diego, 2002.

Ingraham, C.A. and C.A. Pinkert. 2003. Developmental fate of mitochondria microinjected into murine zygotes. Mitochondrion 3, 39-46.

McKenzie, M., I.A. Trounce, C.A. Cassar and C.A. Pinkert. 2004. Production of homoplasmic xenomitochondrial mice. Proc. Natl. Acad. Sci. USA 101, 1685-90.

Trounce, I.A., M. McKenzie, C.A. Cassar, C.A. Ingraham, C.A. Lerner, D.A. Dunn, C.OL. Donegan, K. Takeda, W.K. Pogozelski, R.L. Howell and C.A. Pinkert. 2004. Development and initial characterization of xenomitrochondrial mice. J. Bioenerg. Biomembr. 36, 421-427.

Cannon, M.V., C.A. Pinkert and I.A. Trounce. 2004. Xenomitochondrial embryonic stem cells and mice: Modeling human mitochondrial biology and disease. Gene Therapy and Regulation 2:283-300.

Takeda, K., M. Tasai, M. Iwamoto, A. Onishi, T. Tagami, K. Nirasawa, H. Hanada and C.A. Pinkert. 2005. Microinjection of cytoplasm or mitochondria derived from somatic cells affects parthenogenetic development of murine oocytes. Biol. Reprod. 72:1397-404.

Dunn, D.A., D.L. Kooyman and C. A. Pinkert. 2005. Transgenic animals and their impact on the drug discovery industry. Drug Discovery Today 10:757-67.

Pinkert, C.A. and I.A. Trounce. 2005. Animal modeling: From transgenesis to transmitochondrial models. In: C.D. Berdanier (Ed.)Mitochondria in Health and Disease. Oxidative Stress and Disease Series, Vol. 15, pp. 559-80. CRC Press, Boca Raton.

Welle, S., K. Bhatt and C.A. Pinkert. 2006. Myofibrillar protein synthesis in myostatin-deficient mice. Am. J. Physiol Endocrinol. Metab. 290:E409-15.

Trounce, I.A. and C.A. Pinkert.2007. Cybrid models of mtDNA disease and transmission; from cells to mice. In: J.C. St. John (Ed.) The Mitochondrion in the Germline and Early Development. Current Topics in Devel. Biol., Vol. 77, Ch 6, pp. 157-183. Elsevier Inc.

For more publications check out Pub Med

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