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Qiangrong Liang

Researcher at New York Institute of Technology College of Osteopathic Medicine

Publications -  56
Citations -  8955

Qiangrong Liang is an academic researcher from New York Institute of Technology College of Osteopathic Medicine. The author has contributed to research in topics: Autophagy & Mitophagy. The author has an hindex of 32, co-authored 48 publications receiving 7664 citations. Previous affiliations of Qiangrong Liang include San Francisco VA Medical Center & University of Cincinnati.

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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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The transcription factors GATA4 and GATA6 regulate cardiomyocyte hypertrophy in vitro and in vivo.

Qiangrong Liang, +5 more
- 10 Aug 2001 - 
TL;DR: A direct functional role for GATA4 and GATA6 as regulators of cardiomyocyte hypertrophic growth and gene expression is demonstrated and it is demonstrated that cardiac-expressed GATA factors are necessary mediators of this process.
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Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling

Julian C. Braz, +12 more
- 15 May 2003 - 
TL;DR: Observations indicate that reduced p38 signaling in the heart promotes myocyte growth through a mechanism involving enhanced calcineurin-NFAT signaling.
Journal ArticleDOI

The Transcription Factor GATA4 Is Activated by Extracellular Signal-Regulated Kinase 1- and 2-Mediated Phosphorylation of Serine 105 in Cardiomyocytes

Qiangrong Liang, +6 more
- 01 Nov 2001 - 
TL;DR: A molecular pathway whereby MEK1-ERK1/2 signaling regulates cardiomyocyte hypertrophic growth through the transcription factor GATA4 by direct phosphorylation of serine 105, which enhances DNA binding and transcriptional activation is suggested.
Journal ArticleDOI

Reengineering Inducible Cardiac-Specific Transgenesis With an Attenuated Myosin Heavy Chain Promoter

Atsushi Sanbe, +5 more
- 04 Apr 2003 - 
TL;DR: An efficient, experimentally flexible system that enables us to reversibly affect both abundant and nonabundant cardiomyocyte proteins is developed and appears to be robust and can be used to temporally control high levels of cardiac-specific transgene expression.