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Home » ... » - Faculty » Faculty Pages » Griep, Anne E |
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Griep, Anne E
Anne E. Griep
Professor
Research Area: Vertebrate Eye Development. Cell Cycle and Adhesion. Environmental and toxicant damage on function of ocular tissues. Molecular and genetic regulation of cell proliferation, differentiation and apoptosis in the vertebrate eye.
Home Dept: Anatomy, School of Medicine and Public Health
Affiliated Depts: Molecular and Environmental Toxicology
Address
353 Bardeen Labs
Madison, WI 53706
Phone - 608/262-8988 - Email
Research
The coordinated regulation of cell proliferation, differentiation and death is critical for normal development and for maintaining the specialized functions of differentiated tissues in the adult. Failure to maintain proper controls can result in birth defects, diseases of proliferation such as cancer and a host of degenerative diseases. In the Griep lab, we are investigating the genetic pathways and molecular mechanisms through which cell proliferation, death and differentiation are regulated during normal mouse eye development and how disruption of these controls leads to disease. We focus most of our efforts on the lens, but also have interests in other parts of the eye such as the retina and cornea. We use a variety of genetic, molecular, cell biological and embryological techniques, with transgenic and knockout mice and associated tissue culture systems.
Our work has focused on three aspects of how lens differentiation is controlled at the molecular level. First, our work led to the understanding that the tumor suppressor protein pRb is essential for lens cells to withdraw from the cell cycle and differentiation, in part through its regulation of the activity of E2F transcription factors. The pRB family of proteins also appears to be essential for maintaining normal growth rates in the less differentiated, proliferating cells of the lens. More recently our studies have identified a new family of tumor suppressors, that of the discs-large family, DLG, as also being important for regulating normal cell growth and differentiation in the lens. Second, our studies addressed the mechanism of how lens cells eliminate their organelles, which occurs normally as lens cells differentiate. We now understand that certain members of the caspase family of proteases, the proteases that mediate apoptotic responses, are involved in regulating organelle loss. Finally, the FGF signaling pathways appears to be a regulator of multiple stages of lens cell differentiation and survival. Two areas of our current and future work are: (1) further elucidate the mechanisms through which pRB and DLG families of tumor suppressors control growth and differentiation in less differentiated, proliferating cells as well as in the differentiating cells of the lens; and (2) to identify the molecular pathway including caspases and DLG that regulate organelle loss in the lens and the relationship of this pathway to apoptosis. From our work, we hope to learn more about the mechanisms that regulate normal eye development and how dysregulation of these mechanisms can lead to ocular disorders such as cataracts, retinal degeneration and tumor formation.
 Publications- Cotroneo MS, Haag JD, Zan Y, Lopez CC, Thuwajit P, Petukhova GV, Camerini-Otero RD, Gendron-Fitzpatrick A, Griep AE, Murphy CJ, Dubielzig RR, Gould MN. Characterizing a rat Brca2 knockout model. Oncogene. 2006 Sep 11.
- Nguyen MM, Rivera C, Griep AE. Localization of PDZ domain containing proteins Discs Large-1 and Scribble in the mouse eye. Mol Vis. 2005 Dec 28;11:1183-99.
- Balsitis S, Dick F, Lee D, Farrell L, Hyde RK, Griep AE, Dyson N, Lambert PF. Examination of the pRb-dependent and pRb-independent functions of E7 in vivo. J Virol. 2005 Sep;79(17):11392-402.
Check PubMed for other publications by Anne E. Griep
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