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Mei-Yao Lin

Researcher at National Institutes of Health

Publications -  21
Citations -  1854

Mei-Yao Lin is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Axoplasmic transport & Mitochondrion. The author has an hindex of 16, co-authored 21 publications receiving 1435 citations. Previous affiliations of Mei-Yao Lin include Academia Sinica & National Taiwan University.

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GCMa regulates the syncytin-mediated trophoblastic fusion.

TL;DR: GCMa was able to regulatesyncytin gene expression via two GCMa-binding sites upstream of the 5′-long terminal repeat of thesyncytin-harboring HERV-W family member in BeWo and JEG3 cells but not in HeLa cells, which may help to explain the mechanism underlying the cell fusion event specific for syncytiotrophoblast formation.
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Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits

TL;DR: It is shown that reduced mitochondrial motility and energy deficits in injured axons are intrinsic mechanisms contributing to regeneration failure in mature neurons.
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Axonal autophagosomes recruit dynein for retrograde transport through fusion with late endosomes

TL;DR: Late endosome-loaded dynein–snapin complexes drive amphisome retrograde transport upon fusion of autophagosomes with late endosomes in distal axons.
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Regulation of mitochondrial transport in neurons.

TL;DR: This short review provides an updated overview on motor-adaptor machineries that drive and regulate mitochondrial transport and docking receptors that anchor axonal mitochondria in response to the changes in synaptic activity, metabolic requirement, and altered mitochondrial integrity.
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Cul3-KLHL20 Ubiquitin Ligase Governs the Turnover of ULK1 and VPS34 Complexes to Control Autophagy Termination

TL;DR: It is shown that ULK1, a serine/threonine kinase critical for autophagy initiation, is a substrate of the Cul3-KLHL20 ubiquitin ligase, and KLHL20 governs the degradation of ATG13, VPS34, Beclin-1, and ATG14 in prolonged starvation through a direct or indirect mechanism.