Deregulated cell cycle control in lens epithelial cells by expression of inhibitors of tumor suppressor function
| Autor: | Anne E. Griep, Sarah J. Potter, Minh M. Nguyen |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Embryology
Papillomavirus E7 Proteins Apoptosis Mice Transgenic Vacuole Mice Lens Crystalline medicine Cell Adhesion In Situ Nick-End Labeling Animals Cell Cycle Protein Promoter Regions Genetic In Situ Hybridization biology Cell growth Cell Cycle Retinoblastoma protein Gene Expression Regulation Developmental Cell Differentiation Oncogene Proteins Viral Cell cycle Genes p53 Phenotype Crystallins Epithelium Cell biology Repressor Proteins Microscopy Electron medicine.anatomical_structure Microscopy Fluorescence Mutation biology.protein Intracellular Cell Division Developmental Biology |
| Zdroj: | Mechanisms of Development. 112(1-2):101-113 |
| ISSN: | 0925-4773 |
| DOI: | 10.1016/s0925-4773(01)00644-x |
| Popis: | Previous studies have shown that cell cycle proteins such as retinoblastoma protein (pRB) are essential for cell cycle withdrawal in differentiating lens cells. However, little is known about which factors are critical for cell cycle control in the lens epithelial cells. Here we use the K14 promoter to direct expression of E6 and E7, oncogenes from human papillomavirus type 16, which are known to bind and inactivate p53 and pRB, as molecular tools to study cell cycle regulation in the lens epithelium of transgenic mice. Expression of either gene resulted in increased proliferation and apoptosis, and in the case of E6, a unique epithelial phenotype characterized by multilayering and intercellular vacuoles was observed. Lenses from mice expressing E7 mutants, which are defective in inactivating pRB proteins, were normal and the lens phenotype in the E6 mice was p53-independent. Thus, cell proliferation in the lens epithelium is controlled by multiple factors including, but not necessarily limited to, the pRB family. |
| Databáze: | OpenAIRE |
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