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Yunfei Wen

Researcher at University of Texas MD Anderson Cancer Center

Publications -  5
Citations -  5312

Yunfei Wen is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Medicine & Chemistry. The author has an hindex of 3, co-authored 3 publications receiving 4873 citations.

Papers
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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 Article

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

Daniel J. Klionsky, +2459 more
- 01 Jan 2016 - 
Journal ArticleDOI

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

Daniel J. Klionsky, +2522 more
- 01 Jan 2016 - 
TL;DR: Author(s): Klionsky, DJ; Abdelmohsen, K; Abe, A; Abedin, MJ; Abeliovich, H; A Frozena, AA; Adachi, H, Adeli, K, Adhihetty, PJ; Adler, SG; Agam, G; Agarwal, R; Aghi, MK; Agnello, M; Agostinis, P; Aguilar, PV; Aguirre-Ghis
Journal ArticleDOI

Endothelial p130cas confers resistance to anti-angiogenesis therapy

TL;DR: There were inadvertent errors introduced during figure assembly in Figures 2, 4, and 5; the correct images for each case have been located, and the correct versions of the figures now appear online with the article.
Journal ArticleDOI

Endothelial p130cas confers resistance to anti-angiogenesis therapy

TL;DR: Wen et al. as mentioned in this paper found that internalization of VEGFR2/p130cas fragments in endothelial cells, followed by TNKS1BP1-mediated cell death, is responsible for angiogenesis inhibition with AVA therapy.