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Ke Li

Researcher at Peking Union Medical College

Publications -  49
Citations -  7698

Ke Li is an academic researcher from Peking Union Medical College. The author has contributed to research in topics: Autophagy & Pulmonary fibrosis. The author has an hindex of 18, co-authored 46 publications receiving 5817 citations.

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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 (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

Integrated cytokine and metabolite analysis reveals immunometabolic reprogramming in COVID-19 patients with therapeutic implications.

TL;DR: In this paper, the authors perform both metabolomics and cytokine/chemokine profiling on serum samples from healthy controls, mild and severe COVID-19 patients, and delineate their global metabolic and immune response landscape.
Journal ArticleDOI

TRIB3 supports breast cancer stemness by suppressing FOXO1 degradation and enhancing SOX2 transcription

TL;DR: It is reported that expression of the pseudokinase Tribble 3 (TRIB3) positively associates with breast cancer stemness and progression and is a potential therapeutic strategy against TRIB3-overexpressed breast cancer.
Journal ArticleDOI

TRB3 links insulin/IGF to tumour promotion by interacting with p62 and impeding autophagic/proteasomal degradations.

TL;DR: A previously unrecognized tumour-promoting mechanism for stress protein TRB3 is reported, which mediates a reciprocal antagonism between autophagic and proteasomal degradation systems and connects insulin/IGF to malignant promotion.