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Ayumu Sugiura

Researcher at Montreal Neurological Institute and Hospital

Publications -  22
Citations -  2339

Ayumu Sugiura is an academic researcher from Montreal Neurological Institute and Hospital. The author has contributed to research in topics: Mitochondrion & Medicine. The author has an hindex of 13, co-authored 19 publications receiving 1759 citations. Previous affiliations of Ayumu Sugiura include Tokyo University of Pharmacy and Life Sciences & McGill University.

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Journal ArticleDOI

A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles

TL;DR: The Parkinson's disease‐associated proteins Vps35, Parkin, and PINK1 are involved in the biogenesis of a subset of these MDVs, linking this novel trafficking pathway to human disease.
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Parkinson’s Disease-Related Proteins PINK1 and Parkin Repress Mitochondrial Antigen Presentation

TL;DR: A pathway for mitochondrial antigen presentation that relies on the generation and trafficking of mitochondrial-derived vesicles (MDVs) rather than on autophagy/mitophagy is demonstrated.
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Newly born peroxisomes are a hybrid of mitochondrial and ER-derived pre-peroxisomes

TL;DR: It is shown that the essential import receptors Pex3 and Pex14 target mitochondria, where they are selectively released into vesicular pre-peroxisomal structures, thereby providing full import competence in newly born peroxisomes.
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MAPL SUMOylation of Drp1 Stabilizes an ER/Mitochondrial Platform Required for Cell Death

TL;DR: It is demonstrated how interorganellar contacts are dynamically regulated through active SUMOylation during apoptosis, creating a stabilized platform that signals cytochrome c release.
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MITOL regulates endoplasmic reticulum-mitochondria contacts via Mitofusin2.

TL;DR: The mitochondrial ubiquitin ligase MITOL regulates mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) domain formation through mitofusin2 (Mfn2) through a specific interaction between MITOL C-terminal domain and Mfn2 HR1 domain, which is suggested to regulate ER tethering to mitochondria by activating Mfn 2 via K192 ubiquitination.