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Acetylation of mitochondrial proteins by GCN5L1 promotes enhanced fatty acid oxidation in the heart

American journal of physiology. Heart and circulatory physiology, 2017-08, Vol.313 (2), p.H265-H274

2017

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Adropin regulates pyruvate dehydrogenase in cardiac cells via a novel GPCR-MAPK-PDK4 signaling pathway

Redox biology, 2018-09, Vol.18, p.25-32

2018

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Loss of GCN5L1 in cardiac cells disrupts glucose metabolism and promotes cell death via reduced Akt/mTORC2 signaling

Biochemical journal, 2019-06, Vol.476 (12), p.1713-1724

2019

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G-protein coupled receptor 19 (GPR19) knockout mice display sex-dependent metabolic dysfunction

Scientific reports, 2023-04, Vol.13 (1), p.6134-6134, Article 6134

2023

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Adropin reduces blood glucose levels in mice by limiting hepatic glucose production

Physiological reports, 2019-04, Vol.7 (8), p.e14043-n/a

2019

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GCN5L1 impairs diastolic function in mice exposed to a high fat diet by restricting cardiac pyruvate oxidation

Physiological reports, 2022-08, Vol.10 (15), p.e15415-n/a

2022

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Calreticulin expression in human cardiac myocytes induces ER stress‐associated apoptosis

Physiological reports, 2020-04, Vol.8 (8), p.e14400-n/a

2020

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Reduced acetylation of TFAM promotes bioenergetic dysfunction in the failing heart

iScience, 2023-06, Vol.26 (6), p.106942, Article 106942

2023

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Diet-induced obese mice are resistant to improvements in cardiac function resulting from short-term adropin treatment

Current research in physiology, 2022-01, Vol.5, p.55-62

2022

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Increased fatty acid oxidation enzyme activity in the hearts of mice fed a high fat diet does not correlate with improved cardiac contractile function

Current research in physiology, 2020-12, Vol.3, p.44-49

2020

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Loss of GCN5L1 in cardiac cells limits mitochondrial respiratory capacity under hyperglycemic conditions

Physiological reports, 2019-04, Vol.7 (8), p.e14054-n/a

2019

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Rad GTPase Deletion Increases L‐type Calcium Channel Current Leading to Increased Cardiac Contraction

Journal of the American Heart Association, 2013-12, Vol.2 (6), p.e000459-n/a

2013

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Validation of GCN5L1/BLOC1S1/BLOS1 antibodies using knockout cells and tissue

Biochemical journal, 2024-05, Vol.481 (10), p.643-651

2024

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GPER-dependent estrogen signaling increases cardiac GCN5L1 expression

American journal of physiology. Heart and circulatory physiology, 2022-05, Vol.322 (5), p.H762-H768

2022

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Adropin treatment restores cardiac glucose oxidation in pre-diabetic obese mice

Journal of molecular and cellular cardiology, 2019-04, Vol.129, p.174-178

2019

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Myocardial brain-derived neurotrophic factor regulates cardiac bioenergetics through the transcription factor Yin Yang 1

Cardiovascular research, 2023-03, Vol.119 (2), p.571-586

2023

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The protein acetylase GCN5L1 modulates hepatic fatty acid oxidation activity via acetylation of the mitochondrial β-oxidation enzyme HADHA

The Journal of biological chemistry, 2018-11, Vol.293 (46), p.17676-17684

2018

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GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress

Cellular signalling, 2024-04, Vol.116, p.111065-111065, Article 111065

2024

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Cardiomyocyte-specific deletion of GCN5L1 in mice restricts mitochondrial protein hyperacetylation in response to a high fat diet

Scientific reports, 2020-06, Vol.10 (1), p.10665-10665, Article 10665

2020

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Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome

American Journal of Physiology: Cell Physiology, 2021-09, Vol.321 (3), p.C519-C534

2021

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Rad GTPase Deletion Attenuates Post-Ischemic Cardiac Dysfunction and Remodeling

JACC. Basic to translational science, 2018-02, Vol.3 (1), p.83-96

2018

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Cardiac-specific deletion of GCN5L1 restricts recovery from ischemia-reperfusion injury

Journal of molecular and cellular cardiology, 2019-04, Vol.129, p.69-78

2019

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Phosphoproteomic analysis identifies phospho-Threonine-17 site of phospholamban important in low molecular weight isoform of fibroblast growth factor 2-induced protection against post-ischemic cardiac dysfunction

Journal of molecular and cellular cardiology, 2020-11, Vol.148, p.1-14

2020

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Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging

American journal of physiology. Heart and circulatory physiology, 2015-10, Vol.309 (8), p.H1336-H1345

2015

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Reactive oxygen species in cardiac electrophysiology: loss of Scn1b increases susceptibility to oxidative stress and drives a pro-arrhythmic phenotype

American journal of physiology. Heart and circulatory physiology, 2024-08

2024

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Acetylation of mitochondrial proteins by GCN5L1 promotes enhanced fatty acid oxidation in the heart

Adropin regulates pyruvate dehydrogenase in cardiac cells via a novel GPCR-MAPK-PDK4 signaling pathway

Loss of GCN5L1 in cardiac cells disrupts glucose metabolism and promotes cell death via reduced Akt/mTORC2 signaling

G-protein coupled receptor 19 (GPR19) knockout mice display sex-dependent metabolic dysfunction

Adropin reduces blood glucose levels in mice by limiting hepatic glucose production

GCN5L1 impairs diastolic function in mice exposed to a high fat diet by restricting cardiac pyruvate oxidation

Calreticulin expression in human cardiac myocytes induces ER stress‐associated apoptosis

Reduced acetylation of TFAM promotes bioenergetic dysfunction in the failing heart

Diet-induced obese mice are resistant to improvements in cardiac function resulting from short-term adropin treatment

Increased fatty acid oxidation enzyme activity in the hearts of mice fed a high fat diet does not correlate with improved cardiac contractile function

Loss of GCN5L1 in cardiac cells limits mitochondrial respiratory capacity under hyperglycemic conditions

Rad GTPase Deletion Increases L‐type Calcium Channel Current Leading to Increased Cardiac Contraction

Validation of GCN5L1/BLOC1S1/BLOS1 antibodies using knockout cells and tissue

GPER-dependent estrogen signaling increases cardiac GCN5L1 expression

Adropin treatment restores cardiac glucose oxidation in pre-diabetic obese mice

Myocardial brain-derived neurotrophic factor regulates cardiac bioenergetics through the transcription factor Yin Yang 1

The protein acetylase GCN5L1 modulates hepatic fatty acid oxidation activity via acetylation of the mitochondrial β-oxidation enzyme HADHA

GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress

Cardiomyocyte-specific deletion of GCN5L1 in mice restricts mitochondrial protein hyperacetylation in response to a high fat diet

Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome

Rad GTPase Deletion Attenuates Post-Ischemic Cardiac Dysfunction and Remodeling

Cardiac-specific deletion of GCN5L1 restricts recovery from ischemia-reperfusion injury

Phosphoproteomic analysis identifies phospho-Threonine-17 site of phospholamban important in low molecular weight isoform of fibroblast growth factor 2-induced protection against post-ischemic cardiac dysfunction

Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging

Reactive oxygen species in cardiac electrophysiology: loss of Scn1b increases susceptibility to oxidative stress and drives a pro-arrhythmic phenotype

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