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Mari L. Shinohara

Researcher at Duke University

Publications -  88
Citations -  14159

Mari L. Shinohara is an academic researcher from Duke University. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 37, co-authored 80 publications receiving 11727 citations. Previous affiliations of Mari L. Shinohara include Dartmouth College & State University of New York System.

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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.
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Neuroinflammation in Alzheimer's disease

Michael T. Heneka, +41 more
- 01 Apr 2015 - 
TL;DR: Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction.
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Metabolic programming and PDHK1 control CD4+ T cell subsets and inflammation

Valerie A. Gerriets, +21 more
- 02 Jan 2015 - 
TL;DR: In this article, the authors evaluated CD4+ T cell populations in murine models and determined that inflammatory T cells maintain high expression of glycolytic genes, while Tregs are oxidative and require mitochondrial electron transport to proliferate and differentiate.
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Analysis of regulatory CD8 T cells in Qa-1-deficient mice

Dan Hu, +5 more
- 18 Apr 2004 - 
TL;DR: A Qa-1-dependent T cell–T cell inhibitory interaction that prevents the pathogenic expansion of autoreactive CD4 T cell populations and consequent autoimmune disease is delineated.
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Osteopontin expression is essential for interferon-α production by plasmacytoid dendritic cells

Mari L. Shinohara, +6 more
- 09 Apr 2006 - 
TL;DR: It is shown that Opn deficiency substantially reduced Toll-like receptor 9 (TLR9)–dependent IFN-α responses but spared expression of transcription factor NF-κB–dependent proinflammatory cytokines.