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Jennifer Martinez

Researcher at National Institutes of Health

Publications -  72
Citations -  14551

Jennifer Martinez is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Autophagy & Innate immune system. The author has an hindex of 32, co-authored 69 publications receiving 10811 citations. Previous affiliations of Jennifer Martinez include St. Jude Children's Research Hospital.

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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

Molecular definitions of autophagy and related processes

Lorenzo Galluzzi, +62 more
- 03 Jul 2017 - 
TL;DR: A panel of leading experts in the field attempts here to define several autophagy‐related terms based on specific biochemical features to formulate recommendations that facilitate the dissemination of knowledge within and outside the field of autophagic research.
Journal ArticleDOI

Parkin and PINK1 mitigate STING-induced inflammation

TL;DR: Results support a role for PINK1- and parkin-mediated mitophagy in restraining innate immunity and the loss of dopaminergic neurons from the substantia nigra pars compacta and the motor defect observed in aged Prkn−/−;mutator mice are rescued by loss of STING, suggesting that inflammation facilitates this phenotype.