We transiently expressed wild-type and mutant forms of polyQ disease proteins, Ataxin-1 (Atxn1, the causative gene product for spinocerebellar ataxia type-1, SCA1), Ataxin-7 (Atxn7, the causative gene product for spinocerebellar ataxia type-7, SCA7), huntingtin (Htt, the causative gene product for Huntington’s disease, HD), and androgen receptor (AR, the causative gene product for spinal bulbar muscular atrophy/Kennedy’s disease, SBMA/KD), with or without EGFP-PQBP3, in HeLa cells (Fig. 10A). This evidence concerns the gene NOL7 and Huntington disease.