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Kerri Kluetzman, Ph.D.

Kerri Kluetzman, Ph.D.

Research Scientist
Ph.D., Biomedical Sciences, State University of New York-Albany
M.S., Bacteriology, University of Wisconsin, Madison
(518) 474-6154

Research Interests

The primary objectives of this lab are to combine expertise in transgenic technologies with reproductive sciences in an effort to generate relevant mouse models and to study developmental and genetic origins of disease. Successful reproduction relies on high quality gametogenesis and complex networks of tightly regulated signaling cascades can have a profound impact on fertilization and fetal development. Genetic determinants contribute significantly, however, the environments in which these events occur both in vitro (e.g. in vitro fertilization) and in vivo (uterine environment) also play an important role in influencing fetal development and offspring phenotype. In addition to standard transgenic services, ongoing collaborations are designed to identify and define factors that contribute to successful fertilization and fetal developmental disorders.

Select Publications

Jia K, Li L, Liu Z, Hartog M, Kluetzman K, Zhang QY, Ding X.
Generation and characterization of a novel CYP2A13--transgenic mouse model.
Drug Metab Dispos.
Dias JA, Campo B, Weaver BA, Watts J, Kluetzman K, Thomas RM, Bonnet B, Mutel V, Poli SM.
Inhibition of follicle-stimulating hormone-induced preovulatory follicles in rats treated with a nonsteroidal negative allosteric modulator of follicle-stimulating hormone receptor.
Biol Reprod.
Zhang YB, Gao DH, Kluetzman K, Mendoza A, Bolivar VJ, Reilly A, Jolly JK, Lawrence DA.
The maternal autoimmune environment affects the social behavior of offspring.
Journal of Neuroimmunology.
Wei Y, Li L, Zhou X, Zhang QY, Dunbar A, Liu F, Kluetzman K, Yang WZ, Ding XX.
Generation and Characterization of a Novel Cyp2a(4/5)bgs-Null Mouse Model.
Drug Metabolism & Disposition.
Kluetzman, K. S., Thomas, R. M., Nechamen, C. A. and Dias, J. A.
Decreased degradation of internalized follicle-stimulating hormone caused by mutation of aspartic acid 6.30(550) in a protein kinase-CK2 consensus sequence in the third intracellular loop of human follicle-stimulating hormone receptor.
Biology of Reproduction.