Author

Thomas L. Lynch

Cedars-Sinai Medical CenterORCID 0000-0002-5214-3631Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetics· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

Sakthivel SadayappaniD· 2 shared Akhil BabyiD· 1 shared Aleksandra BinekiD· 1 shared Amanda C. GarfinkeliD· 1 shared Angela C. Tai· 1 shared Barbara A. McDonoughiD· 1 shared Brent Cernyar· 1 shared Charles S RedwoodiD· 1 shared

Activity by Year

2018-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersPhysiology

Sakthivel SadayappanORCID

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2 papers

Recent·Most cited

PhysiologyBasic Research in CardiologyPeer-reviewedAug 5, 2026

Fast skeletal myosin binding protein-C expression exacerbates dysfunction in heart failure

James W. McNamara, Taejeong Song, Perwez Alam…·Sakthivel Sadayappan

This study investigates the role of fast skeletal myosin binding protein-C in heart failure, finding that its expression exacerbates cardiac dysfunction and that its deletion improves heart function.

2 citationstop 4%

mouseexperimental assay

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GeneticsbioRxivPreprintApr 18, 2018

MYBPC3 Mutations cause Hypertrophic Cardiomyopathy by Dysregulating Myosin: Implications for Therapy

Christopher N. Toepfer, Hiroko Wakimoto, Amanda C. Garfinkel…·Christine E. Seidman

The paper shows that MYBPC3 mutations disrupt myosin relaxation states, leading to hyper-contractility in HCM, and that targeting myosin can alleviate these effects.

2 citations

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