Author

I. Scott

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Physiology· 6 Cell Biology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 8 Organism:mouse· 7 Research Focus:cell type annotation· 5 Research Focus:metabolism & bioenergetics· 4 Assay:proteomics· 4 Research Focus:differential expression· 3 Research Focus:cell signaling & trafficking· 2 Assay:metabolomics· 2

Frequent Co-Authors

D. Thapa· 7 shared J. R. Manning· 7 shared M. W. Stoner· 7 shared P. Bugga· 5 shared B. Xie· 4 shared M. J. Jurczak· 4 shared M. Zhang· 4 shared B. A. Mushala· 2 shared

Activity by Year

2019-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

7 shared papersPhysiology

D. Thapa

Mutual co-authors in cluster

Author profile →

8 papers

Recent·Most cited

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

P. Bugga, J. R. Manning, B. A. Mushala, M. W. Stoner, J. Sembrat, I. Scott

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.

bioRxiv · Oct 26, 2023Cell Biology

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

P. Bugga, M. Stoner, J. Manning, B. Mushala, D. Thapa, I. Scott

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

bioRxiv · Jul 21, 2023Cell Biology

Reduced acetylation of TFAM promotes bioenergetic dysfunction in the failing heart

M. Zhang, N. Feng, D. Thapa, M. W. Stoner, J. R. Manning, C. F. McTiernan, X. Yang, Z. Peng, M. J. Jurczak, D. Guimaraes, S. Shiva, B. A. Kaufman, M. N. Sack, I. Scott

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

bioRxiv · Oct 31, 2022Physiology

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

B. A. S. Mushala, B. Xie, I. Sipula, M. W. Stoner, D. Thapa, J. R. Manning, P. Bugga, A. M. Vandevender, M. J. Jurczak, I. Scott

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.

bioRxiv · Oct 29, 2022Physiology

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

D. Thapa, B. Xie, B. A. Mushala, M. Zhang, J. R. Manning, P. Bugga, M. W. Stoner, M. J. Jurczak, I. Scott

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.

bioRxiv · Oct 15, 2021Physiology

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

J. R. Manning, D. Thapa, M. Zhang, M. W. Stoner, J. C. Sembrat, M. Rojas, I. Scott

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.

bioRxiv · Sep 20, 2021 · PreprintPhysiology

GCN5L1 promotes diastolic dysfunction by inhibiting cardiac pyruvate oxidation

D. Thapa, P. Bugga, B. A. S. Mushala, J. R. Manning, M. W. Stoner, B. McMahon, X. Zeng, P. Cantrell, N. Yates, B. Xie, L. R. Edmunds, M. J. Jurczak, I. Scott

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.

bioRxiv · Sep 7, 2021 · PreprintPhysiology

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

D. Thapa, J. R. Manning, M. W. Stoner, M. Zhang, B. Xie, M. N. Sack, I. Scott

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

bioRxiv · Dec 17, 2019 · PreprintPhysiology