I. Scott

GCN5L1 inhibits pyruvate dehydrogenase phosphorylation during cardiac ischemia- reperfusion injury

This study shows that GCN5L1 loss increases pyruvate dehydrogenase phosphorylation, inhibiting glucose oxidation and worsening myocardial damage during ischemia-reperfusion injury.

TCA Cycle Dysfunction and Amino Acid Catabolism Drive Hepatic Steatosis in Mice with HFpEF

This study shows that TCA cycle dysfunction and amino acid catabolism in mice with HFpEF drive hepatic steatosis similar to human NAFLD.

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

This study shows GCN5L1 prevents Rictor degradation in cardiac cells under hypoxia by acetylating Rictor, thereby maintaining Akt/mTORC2 signaling and protecting against ischemic injury.

Validation of GCN5L1/BLOC1S1/BLOS1 Antibodies Using Knockout Cells and Tissue

The paper validates GCN5L1 antibodies using knockout cells and tissue, finding that two-thirds of commercially available antibodies fail to reliably detect the protein.

Reduced acetylation of TFAM promotes bioenergetic dysfunction in the failing heart

This study shows that reduced GCN5L1 expression in the failing heart leads to mitochondrial dysfunction and decreased bioenergetic output.

G-PROTEIN COUPLED RECEPTOR 19 (GPR19) KNOCKOUT MICE DISPLAY SEX-DEPENDENT METABOLIC DYSFUNCTION

This study shows that GPR19 knockout mice exhibit sex-dependent metabolic dysfunction, with males showing glucose intolerance and liver enlargement on a high-fat diet.

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

This study shows that short-term adropin treatment does not improve cardiac function in diet-induced obese mice, but reduces inhibitory phosphorylation of pyruvate dehydrogenase in cardiomyocytes.

GPER-dependent estrogen signaling increases cardiac GCN5L1 expression and MCAD activity

This study shows that estrogen signaling through GPER increases GCN5L1 expression and MCAD activity in cardiac cells, affecting mitochondrial enzyme acetylation and metabolic fuel utilization.

GCN5L1 promotes diastolic dysfunction by inhibiting cardiac pyruvate oxidation

This study identifies GCN5L1 as a regulator of cardiac pyruvate oxidation, showing its role in promoting diastolic dysfunction through inhibition of PDH complex acetylation in aged obese mice.

Cardiomyocyte-Specific Deletion of GCN5L1 in Mice Limits Ex Vivo Cardiac Functional Decline in Response to a High Fat Diet

This study shows that deleting GCN5L1 in cardiomyocytes reduces cardiac functional decline in HFD mice by enhancing substrate flexibility and reducing oxidative damage.