Inhibition of O-GlcNAcase in perfused rat hearts by NAG-thiazolines at the time of reperfusion is cardioprotective in an O-GlcNAc-dependent manner. (Q34357844)

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English	Inhibition of O-GlcNAcase in perfused rat hearts by NAG-thiazolines at the time of reperfusion is cardioprotective in an O-GlcNAc-dependent manner.	scientific article

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scholarly article

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13 February 2020

Inhibition of O-GlcNAcase in perfused rat hearts by NAG-thiazolines at the time of reperfusion is cardioprotective in an O-GlcNAc-dependent manner (English)

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13 February 2020

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13 February 2020

author name string

Boglarka Laczy

1

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13 February 2020

Charlye A Brocks

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13 February 2020

Istvan Wittmann

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13 February 2020

John C Chatham

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publication date

10 September 2010

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13 February 2020

American Journal of Physiology Heart and Circulatory Physiology

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13 February 2020

299

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13 February 2020

H1715-27

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13 February 2020

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13 February 2020

Mechanism, Structure, and Inhibition of O-GlcNAc Processing Enzymes

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Elevation of Global O-GlcNAc Levels in 3T3-L1 Adipocytes by Selective Inhibition of O-GlcNAcase Does Not Induce Insulin Resistance

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Myocardial reperfusion injury.

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Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis

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Glucosamine cardioprotection in perfused rat hearts associated with increased O-linked N-acetylglucosamine protein modification and altered p38 activation

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Impact of Type 2 diabetes and aging on cardiomyocyte function and O-linked N-acetylglucosamine levels in the heart

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Glutamine-induced protection of isolated rat heart from ischemia/reperfusion injury is mediated via the hexosamine biosynthesis pathway and increased protein O-GlcNAc levels

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Glucosamine protects neonatal cardiomyocytes from ischemia-reperfusion injury via increased protein-associated O-GlcNAc

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Cell signaling, the essential role of O-GlcNAc!

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Increased hexosamine biosynthesis and protein O-GlcNAc levels associated with myocardial protection against calcium paradox and ischemia

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10.1152/AJPHEART.00337.2010

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