PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11719247-5	2001	Recently, the transglutaminase activity has been hypothesized to be involved in the pathogenetic mechanisms responsible for the formation of cellular inclusions present in Huntington disease and in all the other polyglutamine (polyQ) diseases hitherto identified, such as spinobulbar muscular atrophy or Kennedy disease, spinocerebellar ataxias (SCA-1, SCA-2, SCA-3 or Machado-Joseph disease, SCA-6 and SCA-7) and dentatorubropallidoluysian atrophy.	polyglutamine	227-232	ataxin 2	Homo sapiens	353-358