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David W Li

Researcher at Sun Yat-sen University

Publications -  93
Citations -  1990

David W Li is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: SUMO protein & Regulation of gene expression. The author has an hindex of 24, co-authored 88 publications receiving 1762 citations. Previous affiliations of David W Li include University of Nebraska Medical Center & Hunan Normal University.

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Calcium-activated RAF/MEK/ERK Signaling Pathway Mediates p53-dependent Apoptosis and Is Abrogated by αB-Crystallin through Inhibition of RAS Activation

TL;DR: A partial explanation for the lack of spontaneous tumor in the lens is provided, a novel signaling pathway for calcium-induced apoptosis is presented, and a novel antiapoptotic mechanism for alphaB-crystallin is presented.
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Human alphaA- and alphaB-crystallins prevent UVA-induced apoptosis through regulation of PKCalpha, RAF/MEK/ERK and AKT signaling pathways.

TL;DR: Together, the results for the first time reveal that by regulating multiple signaling pathways the two α-crystallins can prevent stress-induced apoptosis through different mechanisms.
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Human bcl-2 Gene Attenuates the Ability of Rabbit Lens Epithelial Cells against H2O2-induced Apoptosis through Down-regulation of the αB-crystallin Gene *

TL;DR: The introduction of the human bcl-2 gene into an immortalized rabbit lens epithelial cell line and down-regulation of the αB-crystallin gene reveal that BCL-2 can regulate gene expression in rabbit lenses epithelial cells and reduce resistance to H2O2-induced apoptosis.
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Human telomerase accelerates growth of lens epithelial cells through regulation of the genes mediating RB/E2F pathway.

TL;DR: The results suggest that hTERT, when overexpressed in human lens epithelial cells, accelerates cell growth rate through regulation of RB/E2F pathway and possibly other genes.
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Apoptosis in lens development and pathology.

TL;DR: Both in vitro and in vivo studies have shown that treatment of adult lens with stress factors induces apoptosis of lens epithelial cells, which is followed by cataractogenesis.