Thesis (M.A.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / The gene Myh9 encodes non-muscle myosin heavy chain I lA, an essential podocyte cytoskeleton structural protein. Abnormalities in the MYH9 gene are associated with chronic kidney disease (common in people of African ancestry) and rare hereditary autosomal dominant syndromes. In the current study, preexisting heterozygous Myh9 knockout mice aged 9 and 17 months were investigated to assess the biological role of the gene Myh9 product, non-muscle myosin IIA, in kidney structure and function. The objective was to determine the effects of potentially decreased expression of Myh9 genetic alteration and the role of Myh9 in the pathogenesis of chronic kidney disease (especially focal segmental glomerulosclerosis), and to develop a model to further study Myh9- related kidney disorders. Our results demonstrated that deletion of one allele of Myh9 in 129/Sv mice had no effect on the kidney structure compared with wildtype mice despite a significant decrease in expression of Myh9 in the heterozygous mice. / 2031-01-01
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/34450 |
| Date | January 2011 |
| Creators | Belghasem, Mostafa |
| Publisher | Boston University |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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