Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences. (Articolo in rivista)

Type
Label
  • Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences. (Articolo in rivista) (literal)
Anno
  • 2011-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.4161/cib.4.3.15160 (literal)
Alternative label
  • Zampese, Enrico; Fasolato, Cristina; Pozzan, Tullio; Pizzo, Paola (2011)
    Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences.
    in Communicative & integrative biology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Zampese, Enrico; Fasolato, Cristina; Pozzan, Tullio; Pizzo, Paola (literal)
Pagina inizio
  • 357 (literal)
Pagina fine
  • 60 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://www.ncbi.nlm.nih.gov/pubmed/21980580 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 4 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 3 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Biomedical Sciences; University of Padova and CNR Institute of Neuroscience; Padova, Italy (literal)
Titolo
  • Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences. (literal)
Abstract
  • Presenilin (PS) mutations are the main cause of Familial Alzheimer's Disease (FAD) and have been demonstrated to cause an imbalance of intracellular Ca(2+) homeostasis. Though PS1 and 2 are generally considered to behave similarly in terms of their effects on Ca(2+) handling, we have recently described a novel function, which is unique to PS2, i.e., the modulation of ER-mitochondria juxtaposition. Accordingly, PS2, but not PS1, affects the Ca(2+) cross-talk between these organelles, a key feature in determining cell fate. In particular, PS2 overexpression, and more drastically that of FAD-linked PS2 mutants, strongly increases the interaction between ER and mitochondria, thus facilitating mitochondrial Ca(2+) uptake. The likely mechanisms behind this phenomenon and its potential effects in cell physiology and pathology are discussed. (literal)
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