Author

A. S. Adhikari

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· 2

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

D. V. Trivedi· 2 shared J. A. Spudich· 2 shared K. M. Ruppel· 2 shared S. S. Sarkar· 2 shared D. Bernstein· 1 shared D. Song· 1 shared K. B. Kooiker· 1 shared M. M. Morck· 1 shared

Activity by Year

2019-2019 · peak 2/yr

Co-Author Collaboration Network

9 top collaborators · 30 mutual co-author links

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2 shared papersBiochemistry

D. V. Trivedi

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2 papers

Recent·Most cited

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