Author

D. A. Winkelmann

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:drug response / drug discovery· 1 Organism:human· 1 Approach:microscopy & imaging analysis· 1 Research Focus:protein folding & dynamics· 1 Assay:proteomics· 1

Frequent Co-Authors

B. Barua· 2 shared E. M. Ostap· 2 shared Y. E. Goldman· 2 shared A. Snoberger· 1 shared E. Forgacs· 1 shared H. Shuman· 1 shared J. L. Atherton· 1 shared M. J. Greenberg· 1 shared

Activity by Year

2018-2020 · peak 1/yr

Co-Author Collaboration Network

9 top collaborators · 28 mutual co-author links

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2 shared papersBiophysics

B. Barua

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2 papers

Recent·Most cited

Human hypertrophic cardiomyopathy mutation R712L suppresses the working stroke of cardiac myosin and can be rescued by omecamtiv mecarbil

A. Snoberger, B. Barua, J. L. Atherton, H. Shuman, E. Forgacs, Y. E. Goldman, D. A. Winkelmann, E. M. Ostap

This study shows that the HCM mutation R712L in β-cardiac myosin reduces the working stroke, which is reversed by the drug omecamtiv mecarbil.

bioRxiv · Oct 2, 2020Biophysics

Positive Cardiac Inotrope, Omecamtiv Mecarbil, Activates Muscle Despite Suppressing the Myosin Working Stroke

M. S. Woody, M. J. Greenberg, B. Barua, D. A. Winkelmann, Y. E. Goldman, E. M. Ostap

This study shows that omecamtiv mecarbil increases cardiac output by inhibiting myosin working stroke and enhancing thin filament activation through cooperative mechanisms.

Nature Communications · Sep 21, 2018Peer-reviewedBiophysics