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2002 Scientific Report

  • Text
  • Institute
  • Report
  • Tumors
  • Protein
  • Signaling
  • Michigan
  • Molecular
  • Proteins
  • Laboratory

Publications Albright,

Publications Albright, Craig D., Philip M. Grimley, Raymond T. Jones, and James H. Resau. 2002. Differential effects of TPA and retinoic acid on cell-cell communication in human bronchial epithelial cells. Experimental and Molecular Pathology 72(1): 62–67. Kino, Tomoshige, Roland H. Stauber, James H. Resau, George N. Pavlakis, and George P. Chrousos. 2001. Pathologic human GR mutant has a transdominant negative effect on the wild-type GR by inhibiting its translocation into the nucleus: importance of the ligand-binding domain for intracellular GR trafficking. Journal of Clinical Endocrinology and Metabolism 86(11): 5600–5608. Kort, Eric, Bryon Campbell, and James H. Resau. In press. A shared pathology informatics network. Computer and Programs in Biomedicine. Miura, Koichi, Kerry M. Jacques, Stacey Stauffer, Atsutaka Kubosaki, Kejin Zhu, Dianne Snow Hirsch, James Resau, Yi Zheng, and Paul A. Randazzo. 2002. ARAP1: a point of convergence for Arf and Rho signaling. Molecular Cell 9(1): 109–119. Miura, Koichi, Shoko Miyazawa, Shuichi Furuta, Junji Mitsushita, Keiju Kamijo, Hiroshi Ishida, Toru Miki, Kazumi Suzukawa, James Resau, Terry D. Copeland, and Tohru Kamata. 2001. The Sos1-Rac1 signaling: possible involvement of a vacuolar H + -ATPase E subunit. Journal of Biological Chemistry 276(49): 46276–46283. Qian, Chao-Nan, Xiang Guo, Brian Cao, Eric J. Kort, Chong-Chou Lee, Jindong Chen, Ling-Mei Wang, Wei-Yuan Mai, Hua-Qing Min, Ming-Huang Hong, George F. Vande Woude, James H. Resau, and Bin T. Teh. 2002. Met protein expression level correlates with survival in patients with late-stage nasopharyngeal carcinoma. Cancer Research 62(2): 589–596. From left to right, back row: Hassen, Graves, Moore, Buckner, Resau, Leeser, Hudson front row: Myles, Goolsby 39

Laboratory of Germline Modification Pamela J. Swiatek, Ph.D. Dr. Swiatek received her M.S. (1984) and Ph.D. (1988) degrees in pathology from Indiana University. From 1988 to 1990, she was a Postdoctoral Fellow at the Tampa Bay Research Institute. From 1990 to 1994, she was a Postdoctoral Fellow at the Roche Institute of Molecular Biology in the laboratory of Tom Gridley. From 1994 to 2000, Dr. Swiatek was a Research Scientist and Director of the Transgenic Core Facility at the Wadsworth Center in Albany, New York, and an Assistant Professor in the Department of Biomedical Sciences at the State University of New York at Albany. She joined VARI as a Special Program Investigator, Laboratory of Germline Modification, in August 2000. Staff Kathy Davidson, B.S. Kelly Sisson, B.S. Laboratory Members Student Cassandra Van Dunk Bryn Eagleson, A.A. Bryn Eagleson began her career in laboratory animal services in 1981 with Litton Bionetics at the National Cancer Institute’s Frederick Cancer Research and Development Center (NCI-FCRDC) in Maryland. In 1983, she joined the Johnson & Johnson Biotechnology Center in San Diego, California. In 1988, she returned to the NCI-FCRDC, where she continued to develop her skills in transgenic technology and managed the transgenic mouse colony. During this time she attended Frederick Community College and Hood College in Frederick, Maryland. In 1999, Bryn joined VARI as the Vivarium Director and Transgenic Core Manager. Managerial Staff Jason Martin, RLATG Technical Staff Dawna Dylewski, B.S. Audra Guikema, B.S., L.V.T. Lori Ruff, B.S., RALAT Kristen Van Noord, B.S., RALAT Vivarium Staff Shawn Ballard, A.S., B.A., RALAT Ben Buckrey, B.S. Elissa Boguslawski Research Projects T he Germline Modification Laboratory provides transgenic and gene-targeting technology services to develop mouse models of human disease. These well-established and powerful techniques are used to insert specific genetic changes into the mouse genome in order to study the effect of these mutations in the complex biological environment of a living organism. These changes can include the introduction of a gene into a random site in the genome (transgenics), introduction of a gene into a specific site in the genome (gene knock-in), or the inactivation of a gene already present in the genome (gene knockout). Since these mutations are introduced into the reproductive cells known as the germline, they can be used to study the developmental aspects of gene function associated with inherited genetic diseases. Transgenic mice are produced by injecting small quantities of foreign DNA into a pronucleus of a one-cell fertilized egg. Fertilized eggs contain two pronuclei, one that is derived from the egg and contains the maternal genetic material and one derived from the sperm that contains the paternal genetic material. As development proceeds, these two pronuclei fuse, the genetic material mixes, and the cell proceeds to divide and develop into an embryo. DNA microinjected into a pronucleus randomly integrates into the mouse genome and will theoretically be present in every cell of the resulting organism. Expression of the transgene is controlled by genetic elements called promoters that are genetically engineered into the transgenic DNA. Depending on the selection of the promoter, the transgene can be expressed in every cell of the mouse or in specific cell populations such as neurons, skin cells, or blood cells. Temporal expression of the transgene during development can 40

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