Author

E. P. S. Pratt

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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Cell Biology· 2 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Organism:rat· 2 Assay:electrophysiology· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

K. E. Harvey· 3 shared A. E. Salyer· 2 shared E. K. LaVigne· 2 shared G. H. Hockerman· 2 shared S. Tang· 2 shared G. Hockerman· 1 shared H. Gowher· 1 shared M. S. Dar· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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3 shared papersCell Biology

K. E. Harvey

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Author profile →

3 papers

Recent·Most cited

RyR2 regulates store-operated Ca2+ entry, phospholipase C activity, and electrical excitability in the insulinoma cell line INS-1

K. E. Harvey, S. Tang, E. K. LaVigne, E. P. S. Pratt, G. H. Hockerman

This study shows RyR2 regulates SOCE, PLC activity, and electrical excitability in INS-1 cells by modulating PIP2 levels and Cav channel currents.

bioRxiv · Oct 19, 2022Cell Biology

RyR2/IRBIT regulates insulin gene transcription, insulin content, and secretion in the insulinoma cell line INS-1

K. E. Harvey, E. K. LaVigne, M. S. Dar, E. P. S. Pratt, A. E. Salyer, P. A. Sample, U. K. Aryal, H. Gowher, G. H. Hockerman

Deletion of RyR2 or IRBIT in INS-1 cells reduces insulin content and secretion, with RyR2 also decreasing IRBIT levels and affecting DNA methylation and proteome regulation.

bioRxiv · Nov 24, 2021Cell Biology

Regulation of cAMP accumulation and activity by distinct phosphodiesterase subtypes in INS-1 cells and human pancreatic β-cells

E. P. S. Pratt, K. E. Harvey, A. E. Salyer, s. Tang, G. Hockerman

This study investigates the role of PDE1, PDE3, and PDE4 in regulating cAMP levels and insulin secretion in INS-1 cells and human β-cells, finding that PDE1 inhibition enhances glucose-stimulated insulin secretion and protects against fatty acid toxicity.

bioRxiv · Mar 29, 2019Pharmacology & Toxicology