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John D. MacMicking

Researcher at Yale University

Publications -  56
Citations -  19754

John D. MacMicking is an academic researcher from Yale University. The author has contributed to research in topics: Innate immune system & Nitric oxide synthase. The author has an hindex of 36, co-authored 52 publications receiving 18195 citations. Previous affiliations of John D. MacMicking include Howard Hughes Medical Institute & Rockefeller University.

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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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Nitric oxide and macrophage function

TL;DR: Although the high-output NO pathway probably evolved to protect the host from infection, suppressive effects on lymphocyte proliferation and damage to other normal host cells confer upon NOS2 the same protective/destructive duality inherent in every other major component of the immune response.
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Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase

TL;DR: Mice deficient in inducible nitric oxide synthase (iNOS) were generated to test the idea that iNOS defends the host against infectious agents and tumor cells at the risk of contributing to tissue damage and shock, and found there exist both iN OS-dependent and iNos-independent routes to LPS-induced hypotension and death.
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Identification of nitric oxide synthase as a protective locus against tuberculosis

TL;DR: NOS2(-/-) mice proved highly susceptible, resembling wild-type littermates immunosuppressed by high-dose glucocorticoids, and allowed Mycobacterium tuberculosis to replicate faster in the lungs than reported for other gene-deficient hosts.
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Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase

TL;DR: Induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma and converted resolving ectromelia virus infection into fulminant mousepox in mice.