Author

A. Dawood

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

Biology Disciplines

Click to filter author papers

Biochemistry· 2 Biophysics· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:human· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Assay:imaging· 1

Frequent Co-Authors

K. M. Ruppel· 3 shared D. Bhowmik· 2 shared J. A. Spudich· 2 shared A. Jhingran· 1 shared A. S. Vander Roest· 1 shared B. Pruitt· 1 shared C. Liu· 1 shared D. Bernstein· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 38 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersBiochemistry

K. M. Ruppel

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin allosterically

N. Nandwani, D. Bhowmik, M. C. Childers, R. R. Goluguri, A. Dawood, M. Regnier, J. A. Spudich, K. M. Ruppel

This study investigates how HCM mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin, leading to hypercontractility by destabilizing the OFF-state.

bioRxiv · Feb 29, 2024Biochemistry

Hypertrophic cardiomyopathy mutations in the pliant and light chain-binding regions of the lever arm of human β-cardiac myosin have divergent effects on myosin function

M. Morck, D. Bhowmik, A. Dawood, J. Spudich, K. M. Ruppel

This study examines how mutations in different regions of the β-cardiac myosin lever arm affect motor function and autoinhibition, revealing divergent effects based on mutation location.

bioRxiv · Oct 11, 2021 · PreprintBiochemistry

Hypertrophic cardiomyopathy β-cardiac myosin mutation (P710R) leads to hypercontractility by disrupting super-relaxed state: multiscale measurements and computational modeling

A. S. Vander Roest, C. Liu, M. M. Morck, K. B. Kooiker, G. Jung, D. Song, A. Dawood, A. Jhingran, G. Pardon, S. Ranjbarvaziri, G. Fajardo, M. Zhao, K. S. Campbell, B. Pruitt, J. A. Spudich, , D. Bernstein

This study investigates the P710R mutation in β-cardiac myosin, showing it causes hypercontractility by disrupting the super-relaxed state, using multiscale experiments and modeling.

bioRxiv · Nov 10, 2020 · PreprintBiophysics