Muscular Dystrophy by M. Hegde, A. Ankala
By M. Hegde, A. Ankala
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18, No. 2, (February), pp. 164–166. Brown, LY. & Brown, SA. (2004). Alanine tracts: the expanding story of human illness and trinucleotide repeats. Trends Genet, Vol. 20, No. , Robert, JM. & Fardeau, M. (1990). Oculopharyngeal muscular dystrophy: a census of French families and genealogic study. Rev. Neurol, Vol. 6-7,pp. 425–429 Burdon, RH. (1982). The human heat shock proteins: their induction and possible intracellular functions. , Ashburner, M. and Tissieres, A. , Wahle, E. & Fonseca-Carmo, M.
In a nematode model of OPMD the inhibitor of Sir2 sitinol also showed promising results in protecting muscle cells from apoptosis (Catoire et. , 2008). Gene therapy approach using Bcl2 over expression also rescued OPMD mouse from muscle degeneration (Davies & Rubinsztein, 2011). Several anti amyloid agents such as the disaccharide trehalose, and Congo red also worked in cell culture models of OPMD (Davies et. , 2006). In our laboratory we have used ibuprofen, indomethacin, 8-hydroxy quinoline and ZnSO4 to induce HSP 70 expression in HeLa cells.
Cells were transfected with the appropriate Plasmid DNA after 2 days in the 2 days inthe differentiation medium, cells were lysed and the levels of various muscle proteins, were determined by Western blotting using jappropriate antibodies The Western blots were scanned and the levels of muscle proteins in transfected cells were determined and corrected for the difference in loading and transfection efficiency. The polypeptide levels in PABPN1-A17-GFP-transfected cells relative to that of the PABPN1-A10-GFP expressing cells are given at the bottom of each lane.



