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Richard N. Kitsis

Researcher at Albert Einstein College of Medicine

Publications -  146
Citations -  19345

Richard N. Kitsis is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 55, co-authored 139 publications receiving 14410 citations. Previous affiliations of Richard N. Kitsis include Tufts University & Yeshiva University.

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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
- 23 Jan 2018 - 
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
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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.
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Akt Promotes Survival of Cardiomyocytes In Vitro and Protects Against Ischemia-Reperfusion Injury in Mouse Heart

Yasushi Fujio, +4 more
- 15 Feb 2000 - 
TL;DR: These data are the first documentation that Akt functions to promote cellular survival in vivo, and they indicate that the activation of this pathway may be useful in promoting myocyte survival in the diseased heart.
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The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice.

Orlando F. Bueno, +11 more
- 01 Dec 2000 - 
TL;DR: The results of the present study indicate that the MEK1–ERK1/2 signaling pathway stimulates a physiologic hypertrophy response associated with augmented cardiac function and partial resistance to apoptotsis.