Posttranslational modification of proteins by the small molecule ubiquitin is a key regulatory
event, and the enzymes catalyzing these modifications have been the focus of many studies …

Two central issues in polyglutamine-induced neurodegeneration are the influence of the
normal function of the disease protein and modulation by protein quality control pathways …

We have discovered a ubiquitin (Ub)-specific cysteine protease encoded within the N-
terminal∼ 500 residues of the UL36 gene product, the largest (3164 aa) tegument protein of …

The Josephin domain plays an important role in the cellular functions of ataxin-3, the protein
responsible for the neurodegenerative Machado–Joseph disease. We have determined the …

The polyglutamine-containing neurodegenerative protein ataxin 3 (AT3) has
deubiquitylating activity and binds ubiquitin chains with a preference for chains of four or …

Spinocerebellar ataxia type 3 is a human neurodegenerative disease resulting from
polyglutamine tract expansion. The affected protein, ataxin-3, which contains an N-terminal …

Selective protein degradation by the 26 S proteasome usually requires a polyubiquitin chain
attached to the protein substrate by three classes of enzymes: a ubiquitin-activating enzyme …

Polyglutamine (polyQ) expansions cause neurodegeneration that is associated with protein
misfolding and influenced by functional properties of the host protein. The polyQ disease …

Machado-Joseph's disease is caused by a CAG trinucleotide repeat expansion that is
translated into an abnormally long polyglutamine tract in the protein ataxin-3. Except for the …

Retrotransposons commonly encode a reverse transcriptase (RT), but other functional
domains are variable. The acquisition of new domains is the dominant evolutionary force …