Author

E. A. Assali

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· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:metabolism & bioenergetics· 2 Organism:mouse· 2 Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

I. Sekler· 2 shared M. Taha· 2 shared O. S. Shirihai· 2 shared A. E. Jones· 1 shared G. E. Stutzmann· 1 shared G. Las· 1 shared M. F. Oliveira· 1 shared M. Hershfinkel· 1 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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2 shared papersPhysiology

I. Sekler

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2 papers

Recent·Most cited

NCLX controls hepatic mitochondrial Ca2+ extrusion and couples hormone-mediated mitochondrial Ca2+ oscillations with gluconeogenesis

M. Taha, E. A. Assali, G. E. Stutzmann, O. S. Shirihai, M. Hershfinkel, I. Sekler

This study identifies NCLX as the primary mitochondrial Ca2+ extruder in hepatocytes, linking hormone-mediated mitochondrial Ca2+ oscillations to gluconeogenesis.

bioRxiv · Feb 9, 2024Physiology

NCLX prevents cell death during adrenergic activation of the brown adipose tissue

E. A. Assali, A. E. Jones, M. Veliova, M. Taha, N. Miller, M. Shum, M. F. Oliveira, G. Las, M. Liesa, I. Sekler, O. S. Shirihai

This study identifies NCLX as a critical mitochondrial Na+/Ca2+ exchanger that prevents cell death during adrenergic activation of brown adipose tissue by mitigating Ca2+ overload.

bioRxiv · Nov 6, 2018Physiology