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Carolyn B. Coyne

Researcher at University of Pittsburgh

Publications -  120
Citations -  13342

Carolyn B. Coyne is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Viral replication & Trophoblast. The author has an hindex of 45, co-authored 105 publications receiving 11154 citations. Previous affiliations of Carolyn B. Coyne include University of Alabama at Birmingham & Boston Children's Hospital.

Papers
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Journal ArticleDOI

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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PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity

TL;DR: Recent advances in the understanding of autophagic molecular mechanisms and functions in emergent immunity are reviewed.
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Type III Interferons Produced by Human Placental Trophoblasts Confer Protection against Zika Virus Infection

TL;DR: It is discovered that PHT cells from full-term placentas are refractory to ZIKV infection, and the data suggest that for ZikV to access the fetal compartment, it must evade restriction by trophoblast-derived IFNλ1 and other trophOBlast-specific antiviral factors and/or use alternative strategies to cross the placental barrier.
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Human placental trophoblasts confer viral resistance to recipient cells

TL;DR: This work shows that cultured primary human placental trophoblasts are highly resistant to infection by a number of viruses and confer this resistance to nonplacental recipient cells by exosome-mediated delivery of specific microRNAs (miRNAs) to directly communicate with placental or maternal target cells and regulate their immunity to viral infections.
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Tight junction proteins claudin-1 and occludin control hepatitis C virus entry and are downregulated during infection to prevent superinfection.

TL;DR: It is shown that another TJ protein, occludin, is also required for HCV entry, and Mutational study of CLDN1 revealed that its tight junctional distribution plays an important role in mediating viral entry.