p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca(2+) homeostasis. (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca(2+) homeostasis. (Articolo in rivista) (literal)

Anno

• 2007-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

• 10.1038/sj.cdd.4401997 (literal)

Alternative label

• Pellegrini M.; Finetti F.; Petronilli V.; Ulivieri C.; Giusti F.; Lupetti P.; Giorgio M.; Pelicci P.G.; Bernardi P.; Baldari C.T. (2007)
  p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca(2+) homeostasis.
  in Cell death and differentiation
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Pellegrini M.; Finetti F.; Petronilli V.; Ulivieri C.; Giusti F.; Lupetti P.; Giorgio M.; Pelicci P.G.; Bernardi P.; Baldari C.T. (literal)

Pagina inizio

• 338 (literal)

Pagina fine

• 347 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 14 (literal)

Rivista

• Cell death and differentiation (Rivista)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• Department of Evolutionary Biology, University of Siena, Siena I-53100, Italy / Department of Biomedical Sciences and CNR Institute of Neuroscience, University of Padova, Padova I-35121, Italy / Department of Molecular Oncology, European Institute of Oncology, Milano I-20141, Italy (literal)

Titolo

• p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca(2+) homeostasis. (literal)

Abstract

• p66Shc, a redox enzyme that enhances reactive oxygen species (ROS) production by mitochondria, promotes T cell apoptosis. We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca2+](c). p66Shc expression resulted in profound mitochondrial dysfunction in response to the Ca2+ ionophore A23187, as revealed by dissipation of mitochondrial transmembrane potential, cytochrome c release and decreased ATP levels. p66Shc expression also caused a dramatic alteration in the cells' Ca2+-handling ability, which resulted in Ca2+ overload after A23187 treatment. The impairment in Ca2+ homeostasis was ROS dependent and caused by defective Ca2+ extrusion due at least in part to decreased plasma membrane ATPase (PMCA) expression. Both effects of p66Shc required Ca2+-dependent serine-36 phosphorylation. The mitochondrial effects of p66Shc were potentiated by but not strictly dependent on the rise in [Ca2+](c). Thus, Ca2+-dependent p66Shc phosphorylation causes both mitochondrial dysfunction and impaired Ca2+ homeostasis, which synergize in promoting T cell apoptosis. (literal)

Prodotto di

• Istituto di neuroscienze (IN) (Istituto)
• Neurobiologia e Neuropatologia (ME.P02.005.001) (Modulo)

Autore CNR

• VALERIA PETRONILLI (Unità di personale interno)
• PAOLO BERNARDI (Unità di personale esterno)

Insieme di parole chiave

• Parole chiave di "p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca(2+) homeostasis." (Insieme di parole chiave)

Incoming links:

Autore CNR di

• VALERIA PETRONILLI (Unità di personale interno)
• PAOLO BERNARDI (Unità di personale esterno)

Prodotto

• Istituto di neuroscienze (IN) (Istituto)
• Neurobiologia e Neuropatologia (ME.P02.005.001) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Cell death and differentiation (Rivista)

Insieme di parole chiave di

• Parole chiave di "p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca(2+) homeostasis." (Insieme di parole chiave)