PINK1/Parkin Mediated Mitophagy, Ca2+ Signalling, and ER-Mitochondria Contacts in Parkinson's Disease

International Journal of Molecular Sciences
Lucia BarazzuolTito Calì

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.

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Jul 8, 2020·International Journal of Molecular Sciences·Jae-Min YukEun-Kyeong Jo
Oct 18, 2020·Biomedicines·Maria EjmaGjumrakch Aliev
Feb 9, 2021·Cell Calcium·Salvatore AntonucciNina Kaludercic
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Oct 13, 2021·Neurochemical Research·Abhishek Kumar Mishra, Anubhuti Dixit
Nov 4, 2021·Scientific Reports·Youngshin LimGinam Cho

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Methods Mentioned

BETA
ubiquitination
deubiquitination
GTPase

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