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Zhi-Min Yuan

Researcher at Harvard University

Publications -  113
Citations -  17984

Zhi-Min Yuan is an academic researcher from Harvard University. The author has contributed to research in topics: DNA damage & Phosphorylation. The author has an hindex of 53, co-authored 110 publications receiving 16236 citations. Previous affiliations of Zhi-Min Yuan include University of Texas Health Science Center at San Antonio & University of Texas at San Antonio.

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Journal ArticleDOI

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

p73 is regulated by tyrosine kinase c-Abl in the apoptotic response to DNA damage

Zhi-Min Yuan, +9 more
- 24 Jun 1999 - 
TL;DR: It is shown that c-Abl binds to p73 in cells, interacting through its SH3 domain with the carboxy-terminal homo-oligomerization domain of p73, and that p73 participates in the apoptotic response to DNA damage.
Journal ArticleDOI

Phosphorylation by aurora kinase A induces Mdm2-mediated destabilization and inhibition of p53

Hiroshi Katayama, +10 more
- 01 Jan 2004 - 
TL;DR: It is concluded that aurora Kinase A is a key regulatory component of the p53 pathway and that overexpression of aurora kinase A leads to increased degradation of p53, causing downregulation of checkpoint-response pathways and facilitating oncogenic transformation of cells.
Journal ArticleDOI

Translocation of SAPK/JNK to Mitochondria and Interaction with Bcl-xL in Response to DNA Damage

Surender Kharbanda, +14 more
- 07 Jan 2000 - 
TL;DR: Findings indicate that translocation of SAPK to mitochondria is functionally important for interactions with Bcl-xL in the apoptotic response to genotoxic stress.