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O-GlcNAc signaling attenuates ER stress-induced cardiomyocyte death
Gladys A. Ngoh
,
Tariq Hamid
,
Sumanth D. Prabhu
, Steven P. Jones
Division of Cardiology
Department of Medicine
Center for Cardiovascular Research
Research output
:
Contribution to journal
›
Article
›
peer-review
109
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Scopus citations
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Keyphrases
Endoplasmic Reticulum Stress (ER stress)
100%
Stress-induced
100%
Cardiomyocyte Death
100%
Induced Cardiomyocytes
100%
O-linked N-acetylglucosamine (O-GlcNAc)
100%
O-GlcNAcase
33%
Cardioprotection
22%
Brefeldin A
22%
Induced Cell Death
22%
Protein Activation
22%
O-GlcNAc Transferase
22%
C/EBP Homologous Protein
22%
Overexpression
11%
Unfolded Protein Response
11%
Post-translational Modification
11%
Amino
11%
Per Se
11%
Propidium Iodide
11%
Cell Death Pathways
11%
Myocytes
11%
Pharmacological Inhibitors
11%
Stress Markers
11%
Hypoxia-ischemia
11%
Tunicamycin
11%
Acetamido
11%
Phenylcarbamate
11%
Biochemistry, Genetics and Molecular Biology
Endoplasmic Reticulum Stress
100%
Cardiac Muscle Cell
100%
Cell Death
37%
Transferase
25%
Unfolded Protein Response
12%
Posttranslational Modification
12%
N-Acetylglucosamine
12%
Tunicamycin
12%
Propidium Iodide
12%
Immunology and Microbiology
Endoplasmic Reticulum Stress
100%
Cardiac Muscle Cell
100%
Cell Death
37%
Unfolded Protein Response
12%
Propidium Iodide
12%
Protein Processing
12%
Arm
12%
Neuroscience
Endoplasmic Reticulum Stress
100%
Cell Death
37%
Transferase
25%
Brefeldin A
25%
Unfolded Protein Response
12%
Posttranslational Modification
12%
Myocyte
12%
N Acetylglucosamine
12%
Propidium Iodide
12%
Tunicamycin
12%
Ischemia
12%