CTRL and Huntington disease: A shift in chymotrypsin-like activity was demonstrated from cytosolic fractions to aggregate-containing, precipitated fractions derived from lysates from both a stable HD cell model (expressing huntingtin exon 1 with a 150 polyglutamine repeat) and brain lysates derived from R6/1 mice (expressing exon 1 of the huntingtin gene with a (CAG)116 repeat expansion under control of the huntingtin promoter) [15].