Author

D. Thapa

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

Biology Disciplines

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Physiology· 6 Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 8 Organism:mouse· 7 Research Focus:cell type annotation· 4 Research Focus:metabolism & bioenergetics· 4 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:differential expression· 2 Research Focus:host-pathogen & immune response· 2

Frequent Co-Authors

I. Scott· 7 shared J. R. Manning· 6 shared M. W. Stoner· 6 shared B. Xie· 4 shared M. J. Jurczak· 4 shared M. Zhang· 4 shared P. Bugga· 4 shared B. A. S. Mushala· 2 shared

Activity by Year

2019-2023 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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7 shared papersPhysiology

I. Scott

Mutual co-authors in cluster

Author profile →

8 papers

Recent·Most cited

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

Dysfunctional TRPM8 signalling in the vascular response to environmental cold in ageing.

D. Thapa, J. de Sousa Valente, B. Barrett, F. Argunhan, S. Y. Lee, S. Nikitochkina, X. Kodji, S. D. Brain

This study shows that TRPM8 signaling declines with age, impairing vascular responses to cold in mice.

bioRxiv · May 10, 2021Biochemistry

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