Author

Adam B Lokman

University of OxfordORCID 0000-0002-8717-4550Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Organism:mouse· 1

Frequent Co-Authors

Benjamin DaviesiD· 1 shared Charles S RedwoodiD· 1 shared Charlotte L. Hooper· 1 shared Christopher N. ToepferiD· 1 shared Christopher SemsarianiD· 1 shared Elizabeth OrmondroydiD· 1 shared Evie Singer· 1 shared Gillian DouglasiD· 1 shared

Activity by Year

2025-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperGenetics

Benjamin DaviesORCID

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1 paper

Recent·Most cited

An ALPK3 truncation variant causing autosomal dominant hypertrophic cardiomyopathy is partially rescued by mavacamten

Lisa Leinhos, Paul J. Robinson, Giulia Poloni, Sophie Broadway‐Stringer, Julia Beglov, Adam B Lokman, Gillian Douglas, Sajjad Nuthay, Oveena Fonseka, Manuel Schmid, Evie Singer, Charlotte L. Hooper, Kate L. Thomson, Richard D. Bagnall, Jodie Ingles, , Katja Gehmlich

This study identifies an ALPK3 truncation variant causing HCM and shows that mavacamten partially rescues cardiac contractility and calcium handling defects in a mouse model.

Scientific Reports · Mar 24, 2025Peer-reviewedGenetics