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Grant R. Campbell

Researcher at University of California, San Diego

Publications -  46
Citations -  7887

Grant R. Campbell is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 26, co-authored 42 publications receiving 7075 citations. Previous affiliations of Grant R. Campbell include Boston Children's Hospital & Centre national de la recherche scientifique.

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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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Vitamin D Inhibits Human Immunodeficiency Virus Type 1 and Mycobacterium tuberculosis Infection in Macrophages through the Induction of Autophagy

TL;DR: A biological explanation for the benefits and importance of vitamin D sufficiency in HIV and M. tuberculosis-infected persons is provided, and new insights into novel approaches to prevent and treat HIV infection and related opportunistic infections are provided.
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Hormonally Active Vitamin D3 (1α,25-Dihydroxycholecalciferol) Triggers Autophagy in Human Macrophages That Inhibits HIV-1 Infection

TL;DR: It is found that physiologically relevant concentrations of 1α,25-dihydroxycholecalciferol induce autophagy in human macrophages through a phosphatidylinositol 3-kinase-, ATG-5-, and Beclin-1-dependent mechanism that significantly inhibits HIV-1 replication in a dose-dependent manner.
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Human Immunodeficiency Virus Type 1 Nef Inhibits Autophagy through Transcription Factor EB Sequestration

TL;DR: To the authors' knowledge, this is the first report of a virus modulating TFEB localization and helps to explain how HIV modulates autophagy to promote its own replication and cell survival.