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Jenny P.-Y. Ting

Researcher at University of North Carolina at Chapel Hill

Publications -  351
Citations -  44626

Jenny P.-Y. Ting is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Inflammasome & CIITA. The author has an hindex of 94, co-authored 335 publications receiving 39715 citations. Previous affiliations of Jenny P.-Y. Ting include Duke University & University of Texas Health Science Center at San Antonio.

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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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Inflammasomes: mechanism of action, role in disease, and therapeutics

TL;DR: Increasing evidence in mouse models strongly implicates an involvement of the inflammasome in the initiation or progression of diseases with a high impact on public health, such as metabolic disorders and neurodegenerative diseases.
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Fatty acid-induced NLRP3-ASC inflammasome activation interferes with insulin signaling

TL;DR: It is shown that the saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1β and IL-18 production, which affects insulin sensitivity through tumor necrosis factor–independent and dependent pathways.
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The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

TL;DR: Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge, and a review presents and integrates recent progress in the field.
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The NLRP3 Inflammasome Mediates in vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA

TL;DR: Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS), and inhibition of ROS induction eliminated IL-1beta production in animals during influenza infection.