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Gen Sheng Wu

Researcher at Wayne State University

Publications -  62
Citations -  11138

Gen Sheng Wu is an academic researcher from Wayne State University. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 41, co-authored 59 publications receiving 10241 citations. Previous affiliations of Gen Sheng Wu include University of Pennsylvania.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Arrest of the cell cycle by the tumour-suppressor BRCA1 requires the cdk-inhibitor p21waf1/cip1

Kumaravel Somasundaram, +8 more
- 11 Sep 1997 - 
TL;DR: It is shown that BRCA1 transactivates expression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 in a p53-independent manner, and that B RCA1 inhibits cell-cycle progression into the S-phase following its transfection into human cancer cells.
Journal Article

p53-dependent and -independent Regulation of the Death Receptor KILLER/DR5 Gene Expression in Response to Genotoxic Stress and Tumor Necrosis Factor α

M. Saeed Sheikh, +7 more
- 15 Apr 1998 - 
TL;DR: It is demonstrated that the DR KILLER/DR5 gene is regulated in a p53-dependent and -independent manner during genotoxic and nongenotoxic stress-induced apoptosis and that its induction by TNF-alpha, p53, or DNA damage is not the consequence of apoptosis induced by these agents.
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Notch signaling: an emerging therapeutic target for cancer treatment.

Xun Yuan, +7 more
- 01 Dec 2015 - 
TL;DR: A review of the recent studies and clinical evaluations of the Notch inhibitors in cancer suggests that the pharmacological inhibition of this pathway can overcome chemoresistance.
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Dual Inactivation of Akt and ERK by TIC10 Signals Foxo3a Nuclear Translocation, TRAIL Gene Induction, and Potent Antitumor Effects

Joshua E. Allen, +16 more
- 06 Feb 2013 - 
TL;DR: TIC10 is a small molecule that activates Foxo3a through dual inactivation of Akt and ERK, up-regulates the expression of the TRAIL gene, an endogenous tumor suppressor, and effectively improves the therapeutic properties and utility of TRAIL as an anticancer therapy.