Title : Transglutaminase-dependent formation of protein aggregates as possible biochemical mechanism for polyglutamine diseases.

Pub. Date : 2001 Oct-Nov 1

PMID : 11719247






1 Functional Relationships(s)
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1 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 ataxin 2 Homo sapiens