Leonard Pinsky

TL;DR: The results suggest that by generation of truncated polyglutamine-containing proteins, caspase cleavage may represent a common step in the pathogenesis of each of these neurodegenerative diseases.

TL;DR: It is reported that hAR transactivity and polyGlutamine (polyGln)-tract length are related inversely: n = 0 > 12 > 20 > 40 > 50, and a normal-size polyGln tract represses the transactivational competence of a polyGlngn-free hAR, andPolyGln expansion increases that negative effect.

TL;DR: It is found that a polyglutamine (Gln) expanded AR transactivates an androgen–responsive reporter gene subnormally and causes the AR to lose a function necessary for full androgen sensitivity and to gain a function that is selectively motor neuronotoxic.

TL;DR: The current version of the androgen receptor (AR) gene mutations database is described, and the contribution of CpG sites to the multiplicity of reports of the same mutation in different families is examined.

TL;DR: It is reported the first conclusive evidence that caspase cleavage is a critical step in cytotoxicity ; the expression of the AR with an expanded polyglutamine stretch enhances its ability to induce apoptosis when compared with the normal AR, and a strategy that may be useful to treat neurodegenrative diseases associated with polyglUTamine repeat expansions is suggested.