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- W3009373616 endingPage "1772" @default.
- W3009373616 startingPage "1772" @default.
- W3009373616 abstract "Endoplasmic reticulum (ER)–mitochondria contact sites are critical structures for cellular function. They are implicated in a plethora of cellular processes, including Ca2+ signalling and mitophagy, the selective degradation of damaged mitochondria. Phosphatase and tensin homolog (PTEN)-induced kinase (PINK) and Parkin proteins, whose mutations are associated with familial forms of Parkinson’s disease, are two of the best characterized mitophagy players. They accumulate at ER–mitochondria contact sites and modulate organelles crosstalk. Alterations in ER–mitochondria tethering are a common hallmark of many neurodegenerative diseases including Parkinson’s disease. Here, we summarize the current knowledge on the involvement of PINK1 and Parkin at the ER–mitochondria contact sites and their role in the modulation of Ca2+ signalling and mitophagy." @default.
- W3009373616 created "2020-03-13" @default.
- W3009373616 creator A5015986695 @default.
- W3009373616 creator A5068371692 @default.
- W3009373616 creator A5071829494 @default.
- W3009373616 creator A5083406683 @default.
- W3009373616 date "2020-03-05" @default.
- W3009373616 modified "2023-10-05" @default.
- W3009373616 title "PINK1/Parkin Mediated Mitophagy, Ca2+ Signalling, and ER–Mitochondria Contacts in Parkinson’s Disease" @default.
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