Calcium-dependent cleavage of endogenous wild-type huntingtin in primary cortical neurons. (Articolo in rivista)

Type
Label
  • Calcium-dependent cleavage of endogenous wild-type huntingtin in primary cortical neurons. (Articolo in rivista) (literal)
Anno
  • 2002-01-01T00:00:00+01:00 (literal)
Alternative label
  • Goffredo D., Rigamonti D., Tartari M., De Micheli A., Verderio C., Matteoli M., Zuccato C., Cattaneo E. (2002)
    Calcium-dependent cleavage of endogenous wild-type huntingtin in primary cortical neurons.
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Goffredo D., Rigamonti D., Tartari M., De Micheli A., Verderio C., Matteoli M., Zuccato C., Cattaneo E. (literal)
Pagina inizio
  • 39594 (literal)
Pagina fine
  • 39598 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 277 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Titolo
  • Calcium-dependent cleavage of endogenous wild-type huntingtin in primary cortical neurons. (literal)
Abstract
  • Huntingtos’s disease (HD) is caused by a polyglutamine expansion in the amin-terminal region of huntingtin. Mutant huntingtin is proteolytically cleaved by caspases, generating amino-terminal aggregates wich are toxic for cells. Addition of calpains to total brain homogenates also leads to cleavage of zild-type huntingtin, indicating that proteolysis of mutant and wild-type huntingtin may play a role in HD. Here we report that endogenous wild-type huntingtin is promptly cleaved by calpains in primary neurons. Loss of intact full-length wild-type huntingtin occurs also after exposure of primary neurons to glutamate or 3-nitropropionic acid, which lead to increased intracellular calcium concentration, and could be prevented by calcium chelators and calpains inhibitors. Degradation of wild-type huntingtin by calcium-dependent proteases thus occurs in HD neurons leading to loss of wild-type huntingtin neuroprotecive activity. (literal)
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