Author

D. V. Trivedi

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

Biology Disciplines

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Biochemistry· 3 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:host-pathogen & immune response· 3 Organism:human· 3 Assay:proteomics· 2 Approach:biophysical modeling· 1 Research Focus:drug response / drug discovery· 1 Organism:plant (other)· 1 Research Focus:protein folding & dynamics· 1

Frequent Co-Authors

J. A. Spudich· 3 shared K. M. Ruppel· 3 shared S. S. Sarkar· 3 shared A. S. Adhikari· 2 shared D. Song· 2 shared A. Chakraborty· 1 shared A. Karabina· 1 shared A. Racca· 1 shared

Activity by Year

2018-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersBiochemistry

J. A. Spudich

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Author profile →

4 papers

Recent·Most cited

A small-molecule myosin inhibitor as a targeted multi-stage antimalarial

D. V. Trivedi, A. Karabina, G. Bergnes, A. Racca, H. Wander, S. Jung, N. Mittal, T. Huijs, S. Ouchida, P. V. Ruijgrok, D. Song, S. Wittlin, P. Mukherjee, A. Chakraborty, E. A. Winzeler, , J. Spudich

This paper develops a small-molecule myosin inhibitor, KNX-115, effective against multiple stages of Plasmodium infection with high selectivity and potency.

bioRxiv · Sep 9, 2022 · PreprintPharmacology & Toxicology

The molecular basis of hypercontractility caused by the hypertrophic cardiomyopathy mutations R403Q and R663H

S. S. Sarkar, D. V. Trivedi, M. M. Morck, A. S. Adhikari, S. N. Pasha, K. M. Ruppel, J. A. Spudich

This study investigates how HCM mutations R403Q and R663H in myosin cause hypercontractility by increasing functionally-accessible myosin heads and affecting MyBP-C binding.

bioRxiv · Feb 7, 2019 · PreprintBiochemistry

Hypertrophic cardiomyopathy mutations at the folded-back sequestered β-cardiac myosin S1-S2 and S1-S1 interfaces release sequestered heads and increase myosin enzymatic activity

A. S. Adhikari, D. V. Trivedi, S. S. Sarkar, D. Song, K. B. Kooiker, D. Bernstein, J. A. Spudich, K. M. Ruppel

This study shows HCM mutations at specific myosin interfaces increase accessible heads and myosin activity, contributing to hypercontractility.

bioRxiv · Jan 31, 2019Biochemistry

Mavacamten stabilizes a folded-back sequestered super-relaxed state of β-cardiac myosin

R. L. Anderson, D. V. Trivedi, S. S. Sarkar, M. Henze, W. Ma, H. Gong, C. S. Rogers, F. L. Wong, M. Morck, J. G. Seidman, K. M. Ruppel, T. C. Irving, R. Cooke, E. M. Green, J. A. Spudich

The paper shows that mavacamten stabilizes a folded-back sequestered super-relaxed state of β-cardiac myosin, linking mutations to cardiomyopathy mechanisms.

bioRxiv · Mar 10, 2018Biochemistry