Author

Saffie E. Mohran

University of WashingtonORCID 0000-0003-0728-9882Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:human· 3 Assay:ATAC-seq· 2 Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Michael RegnieriD· 3 shared Ateeqa NaimiD· 2 shared Christian MandryckyiD· 2 shared Farid Moussavi‐HaramiiD· 2 shared Jing ZhaoiD· 2 shared Kristina Bezold KooikeriD· 2 shared Matthew Carter ChildersiD· 2 shared Matvey PilagoviD· 2 shared

Activity by Year

2023-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersBiophysics

Michael RegnierORCID

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3 papers

Recent·Most cited

BiophysicsJournal of Molecular and Cellular CardiologyPeer-reviewedOct 28, 2025

Molecular mechanisms of altered contraction with the β-myosin R403Q mutation in porcine ventricular muscle and a human stem cell-derived cardiomyocyte model.

Sonette Steczina, Saffie E. Mohran, Matthew Carter Childers…·Michael Regnier

This study investigates the R403Q mutation in beta-myosin heavy chain using porcine and human stem cell models, revealing altered contractile properties and mechanisms of hypercontractility and impaired relaxation.

7 citationstop 4%

humanmouse

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BiophysicsbioRxivPreprintMay 14, 2025

Myosin modulator Aficamten inhibits force in cardiac muscle by altering myosin's biochemical activity without changing thick filament structure

Saffie E. Mohran, Kristina Bezold Kooiker, Ateeqa Naim…·Farid Moussavi‐Harami

This paper shows Aficamten inhibits cardiac myosin ATPase without changing thick filament structure, unlike Mavacamten, leading to similar force reduction but different kinetic effects.

3 citations

humanATAC-seq

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Molecular BiologybioRxivPreprintJun 8, 2023

Multi-scale models reveal hypertrophic cardiomyopathy MYH7 G256E mutation drives hypercontractility and elevated mitochondrial respiration

Soah Lee, Alison Schroer Vander Roest, Cheavar A. Blair…·Daniel Bernstein

This study investigates the effects of the MYH7 G256E mutation on myosin function across multiple scales, finding increased hypercontractility and mitochondrial respiration.

2 citations

humanscRNA-seq

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