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Yong Ma

Researcher at Harbin Medical University

Publications -  29
Citations -  10903

Yong Ma is an academic researcher from Harbin Medical University. The author has contributed to research in topics: Apoptosis & In vivo. The author has an hindex of 17, co-authored 28 publications receiving 9395 citations. Previous affiliations of Yong Ma include Johns Hopkins University.

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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.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Genistein potentiates the effect of arsenic trioxide against human hepatocellular carcinoma: role of Akt and nuclear factor-κB.

TL;DR: The results demonstrated that genistein not only potentiated the proliferation-inhibiting and apoptosis-inducing effect of ATO on human HCC cell lines in vitro, but also dramatically augmented its suppressive effect on both tumor growth and angiogenesis in nude mice.
Journal ArticleDOI

Hydroxytyrosol, a natural molecule from olive oil, suppresses the growth of human hepatocellular carcinoma cells via inactivating AKT and nuclear factor-kappa B pathways.

TL;DR: The results show that HT could inhibit proliferation, induce G2/M cell cycle arrest and apoptosis in human HCC cells, and Mechanically, HT could suppress the activation of AKT and nuclear factor-kappa B (NF-κB) pathways.