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Jeffrey Robbins

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  264
Citations -  28548

Jeffrey Robbins is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Myosin & Transgene. The author has an hindex of 77, co-authored 263 publications receiving 25927 citations. Previous affiliations of Jeffrey Robbins include University of Connecticut & Hospital Research Foundation.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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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A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy

Jeffery D. Molkentin, +8 more
- 17 Apr 1998 - 
TL;DR: It is shown that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to the nucleus.
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Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Christopher P. Baines, +11 more
- 31 Mar 2005 - 
TL;DR: Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
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Cardiac Fibrosis: The Fibroblast Awakens.

Joshua G. Travers, +4 more
- 18 Mar 2016 - 
TL;DR: Current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury are summarized, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis are summarized.
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Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis

Xianghai Liao, +8 more
- 04 Apr 2012 - 
TL;DR: A mechanism-based strategy to therapeutically suppress atherosclerosis progression and its clinical sequelae is suggested, suggesting a protective process in oxidatively stressed macrophages relevant to plaque necrosis.