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Robin B. Chan

Researcher at Columbia University Medical Center

Publications -  47
Citations -  3474

Robin B. Chan is an academic researcher from Columbia University Medical Center. The author has contributed to research in topics: Lipid metabolism & Endosome. The author has an hindex of 27, co-authored 41 publications receiving 2753 citations. Previous affiliations of Robin B. Chan include Columbia University & National University of Singapore.

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Comparative lipidomic analysis of mouse and human brain with Alzheimer disease.

TL;DR: In this paper, a system-based approach was employed to determine the lipidome of brain tissues affected by Alzheimer disease using liquid chromatography-mass spectrometry to profile extracts from the prefrontal cortex, entorhinal cortex, and cerebellum of late-onset AD patients.
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Retroviruses human immunodeficiency virus and murine leukemia virus are enriched in phosphoinositides.

TL;DR: Overall, these results suggest that HIV-1 and other retroviruses bud from cholesterol-rich regions of the plasma membrane and exploit matrix/PI(4,5)P2 interactions for particle release from cells.
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Phosphatidylinositol-3-phosphate regulates sorting and processing of amyloid precursor protein through the endosomal system

TL;DR: Phosphatidylinositol-3-phosphate deficiency is established as a contributing factor in Alzheimer's disease and the mechanisms of amyloid precursor protein trafficking through the endosomal system in normal and pathological states are clarified.
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Phospholipase D2 Ablation Ameliorates Alzheimer's Disease-Linked Synaptic Dysfunction and Cognitive Deficits

TL;DR: It is shown that oligomeric Aβ enhances PLD activity in cultured neurons and that this stimulatory effect does not occur upon ablation of PLD2 via gene targeting, which points to specific molecular species of PA as key modulators of AD pathogenesis and identifies PLD 2 as a novel potential target for therapeutics.
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Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease

TL;DR: It is shown that C99, in addition to its localization in endosomes, can also be found in MAM, where it is normally processed rapidly by γ‐secretase, and this change in mitochondrial membrane composition interferes with the proper assembly and activity of mitochondrial respiratory supercomplexes, thereby likely contributing to the bioenergetic defects characteristic of AD.