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Dominic P. Del Re

Researcher at Rutgers University

Publications -  45
Citations -  8342

Dominic P. Del Re is an academic researcher from Rutgers University. The author has contributed to research in topics: Hippo signaling pathway & Signal transduction. The author has an hindex of 21, co-authored 40 publications receiving 7057 citations. Previous affiliations of Dominic P. Del Re include University of California, San Diego & Yeshiva University.

Papers
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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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Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease

TL;DR: The most important conclusion relevant to heart disease is that regulated forms of cardiomyocyte death play important roles in both myocardial infarction with reperfusion (ischemia/reperfusion) and heart failure.
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Mst1 inhibits autophagy by promoting the interaction between Beclin1 and Bcl-2

TL;DR: It is suggested that Mst1 coordinately regulates autophagy and apoptosis by phosphorylating Beclin1 and consequently modulating a three-way interaction among Bcl-2 proteins, Becl in1 and Bax.
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The Rac and Rho Hall of Fame: A Decade of Hypertrophic Signaling Hits

TL;DR: The evolution of knowledge related to Rac1 and RhoA in the context of hypertrophy and heart failure is assessed and the direction that future exploration will lead is highlighted.
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Yes-associated protein isoform 1 (Yap1) promotes cardiomyocyte survival and growth to protect against myocardial ischemic injury*

TL;DR: Yap1 is critical for basal heart homeostasis and that Yap1 deficiency exacerbates injury in response to chronic MI, and the findings suggest increasing cardiomyocyte survival and proliferation may afford protection in vivo against MI injury.