ASC-J9 ameliorates spinal and bulbar muscular atrophy phenotype via degradation of androgen receptor

Article Abstract:

The addition of 5-hydroxy-1,7-bis(3,4-dimethoxyphenyl)-1,4,6-heptatrien-3-one (ASC-J9) is shown to disrupt the interaction between androgen receptor (AR) and its coregulator and also increase the cell survival by decreasing AR-polyQ nuclear aggregation and increasing AR-polyQ degradation in cultured cells. The results have provided a better therapeutic and preventive approach for treating spinal and bulbar muscular atrophy, by disrupting the interaction between AR and AR coregulators.

United States, Causes of, Genetic aspects, Phenotype, Phenotypes, Spinal muscular atrophy

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17-AAG, an Hsp90 inhibitor, ameliorates polyglutamine-mediated motor neuron degeneration

Article Abstract:

The therapeutic effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG), a potent Hsp90 inhibitor, and its ability to degrade polyglutamine-expanded mutant androgen receptor (AR) are examined. The mutant AR showed a higher affinity for Hsp90-p23 and preferentially formed an Hsp90 chaperone complex as compared to wild-type AR.

Health aspects, Motor neurons, Androgens

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Leuprorelin rescues polyglutamine-dependent phenotypes in a transgenic mouse model of spinal and bulbar muscular atrophy

Article Abstract:

The effect of androgen-blockade drugs on the transgenic mouse model was examined. Leuprorelin that seems to be a promising candidate for the treatment of spinal and bulbar muscular atrophy (SBMA) is discussed.

Genetically modified mice, Atrophy, Muscular, Muscular atrophy

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