Author

Saswata S Sarkar

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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Biophysics· 2 Biochemistry· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell signaling & trafficking· 2 Assay:proteomics· 2 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:host-pathogen & immune response· 1 Research Focus:protein folding & dynamics· 1

Frequent Co-Authors

Kathleen M Ruppel· 3 shared James A Spudich· 2 shared Shirley Sutton· 2 shared Arjun S Adhikari· 1 shared Chao Liu· 1 shared Daniel Bernstein· 1 shared Darshan V Trivedi· 1 shared James Spudich· 1 shared

Activity by Year

2016-2016 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersBiophysics

Kathleen M Ruppel

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3 papers

Recent·Most cited

BiophysicsbioRxivAug 9, 2016

Mutations in the catalytic domain of human β-cardiac myosin that cause early onset hypertrophic cardiomyopathy significantly increase the fundamental parameters that determine ensemble force and velocity

Arjun S Adhikari, Kristina B Kooiker, Chao Liu…·Kathleen M Ruppel

This study examines two HCM-causing mutations in human β-cardiac myosin, finding significant increases in actin gliding velocity, intrinsic force, and ATPase activity, indicating a hyper-contractile phenotype.

DOI 10.1016/j.celrep.2016.11.040

humanproteomics

𝕏 PostBluesky

BiophysicsbioRxivJul 26, 2016

Biophysical properties of human β-cardiac myosin with converter mutations that cause hypertrophic cardiomyopathy

Masataka Kawana, Saswata S Sarkar, Shirley Sutton…·James Spudich

The paper analyzes biophysical properties of human β-cardiac myosin with HCM-causing converter domain mutations, finding minimal changes or slightly hypo-contractile profiles, contrasting with clinical hyper-contractility.

DOI 10.1126/sciadv.1601959

humanexperimental assay

𝕏 PostBluesky

BiochemistrybioRxivJul 24, 2016

Beyond the myosin mesa: a potential unifying hypothesis on the underlying molecular basis of hyper-contractility caused by a majority of hypertrophic cardiomyopathy mutations

Suman Nag, Darshan V Trivedi, Saswata S Sarkar…·James A Spudich

This paper proposes a unifying hypothesis that hypertrophic cardiomyopathy mutations increase functionally accessible myosin heads in the sarcomere, leading to hyper-contractility.

DOI 10.1038/nsmb.3408

humanproteomics

𝕏 PostBluesky