Heat Shock Protein 70 Chaperone Overexpression Ameliorates Phenotypes of the Spinal and Bulbar Muscular Atrophy Transgenic Mouse Model by Reducing Nuclear-Localized Mutant Androgen Receptor Protein.

Presents a study which reported that overexpression of the inducible form of human HSP70 markedly ameliorated clinical and pathological phenotypes, and that this amelioration was correlated with the reduction of nuclear-localized mutant androgen receptor (AR) protein complexes in the mouse model of spinal and bulbar muscular atrophy. Materials and methods; Nondeleterious effects of HSP70 overexpression and generation of double-transgenic mice; Colocalization of HSP70 with mutant AR in the nuclei.