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Nai-Di Yang

Researcher at National University of Singapore

Publications -  8
Citations -  1150

Nai-Di Yang is an academic researcher from National University of Singapore. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 7, co-authored 8 publications receiving 899 citations. Previous affiliations of Nai-Di Yang include Nanjing Tech University.

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Targeting the Endocytic Pathway and Autophagy Process as a Novel Therapeutic Strategy in COVID-19.

TL;DR: This mini-review will focus on the importance of the endocytic pathway as well as the autophagy process in viral infection of several pathogenic CoVs inclusive of SARS- coV, MERS-CoV and the new CoV named as severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2), and discuss the development of therapeutic agents by targeting these processes.
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Activation of lysosomal function in the course of autophagy via mTORC1 suppression and autophagosome-lysosome fusion

TL;DR: It is found that suppression of mammalian target of rapamycin activity by starvation or two mTOR catalytic inhibitors (PP242 and Torin1), but not by an allosteric inhibitor (rapamycin), leads to activation of lysosomal function.
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Histone deacetylase inhibitors induce autophagy through FOXO1-dependent pathways

TL;DR: The studies reveal a novel function of FOXO1 in HDACIs-mediated autophagy in human cancer cells and thus support the development of a novel therapeutic strategy by combining HDACs and autophagic inhibitors in cancer therapy.
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Artesunate Induces Cell Death in Human Cancer Cells via Enhancing Lysosomal Function and Lysosomal Degradation of Ferritin

TL;DR: This study demonstrates that ART treatment activates lysosomal function and then promotes ferritin degradation, subsequently leading to the increase of lysOSomal iron that is utilized by ART for its cytotoxic effect on cancer cells.
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(−)-Epigallocatechin-3-Gallate Induces Non-Apoptotic Cell Death in Human Cancer Cells via ROS-Mediated Lysosomal Membrane Permeabilization

TL;DR: A novel mechanism underlying EGCG-induced cell death involving ROS and LMP is revealed, and it is found that E GCG promotes production of intracellular ROS upstream of LMP and cell death, as evidenced by increased level of ROS in cells treated with EGCGs and the protective effects of antioxidant N-acetylcysteine against NAC.