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Min Chen

Researcher at National Institutes of Health

Publications -  131
Citations -  13579

Min Chen is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Gs alpha subunit & Apoptosis. The author has an hindex of 53, co-authored 117 publications receiving 11762 citations. Previous affiliations of Min Chen include University of Southern California & Baylor College of Medicine.

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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.
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Essential role for Nix in autophagic maturation of erythroid cells

Hector Sandoval, +6 more
- 10 Jul 2008 - 
TL;DR: It is suggested that Nix-dependent loss of ΔΨm is important for targeting the mitochondria into autophagosomes for clearance during erythroid maturation, and interference with this function impairs erythyroidmaturation and results in anaemia.
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Effects of a naturally occurring mutation in the hepatitis B virus basal core promoter on precore gene expression and viral replication.

Victor E. Buckwold, +4 more
- 01 Sep 1996 - 
TL;DR: The results of the in vitro study resolve the discrepancy of previous clinical observations and indicate that this double mutation of nucleotides 1762 and 1764 in the BCP suppresses but does not abolish the e antigen phenotype.
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Initiator caspases in apoptosis signaling pathways.

Min Chen, +1 more
- 01 Aug 2002 - 
TL;DR: In this article, the authors investigated the role of caspase activation in the DISC and apoptosome in inducing the onset of death receptor-mediated and mitochondrion-dependent apoptosis.
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Dendritic cell apoptosis in the maintenance of immune tolerance.

Min Chen, +10 more
- 24 Feb 2006 - 
TL;DR: The observation that a defect in DC apoptosis can independently lead to autoimmunity is consistent with a central role for these cells in maintaining immune self-tolerance.