Decreasing levels of mutant, but not normal, huntingtin (HTT) protein remains a major obstacle to treating Huntington's disease (HD). Bauer et al. show that a fusion of polyglutamine-and HSC70–binding motifs specifically targets mutant HTT for degradation by chaperone-mediated autophagy and ameliorates the phenotype of a mouse model of HD.
- Peter O Bauer
- Anand Goswami
- Nobuyuki Nukina
