Author

M. N. Sack

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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Immunology· 2 Physiology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:mouse· 3 Assay:proteomics· 3 Research Focus:cell type annotation· 2 Research Focus:host-pathogen & immune response· 2 Assay:metabolomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

D. Thapa· 2 shared I. Scott· 2 shared J. R. Manning· 2 shared M. W. Stoner· 2 shared M. Zhang· 2 shared A. C. Russo· 1 shared A. K. Gupta· 1 shared B. A. Kaufman· 1 shared

Activity by Year

2019-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersPhysiology

D. Thapa

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

BLOC1S1 control of vacuolar organelle fidelity modulates TH2 cell immunity and allergy susceptibility.

R. Sharma, K. Wu, K. Han, A. C. Russo, P. K. Dagur, C. A. Combs, M. N. Sack

This study shows that BLOC1S1 depletion disrupts mitochondrial integrity, leading to TH2 cell immunity and allergy susceptibility via STING-NF-κB signaling.

bioRxiv · Mar 21, 2024 · PreprintImmunology

The mitochondrial thiolase ACAT1 regulates monocyte/macrophage type I interferon via epigenetic control.

J. Wu, K. SIngh, V. Shing, A. K. Gupta, R. D. Huffstutler, D.-Y. Lee, M. N. Sack

This study shows ACAT1 regulates type I interferon via epigenetic control by linking fatty acid metabolism to histone acetylation in macrophages.

bioRxiv · Jan 29, 2024 · PreprintImmunology

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

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