Author

K. B. Kooiker

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· 1 Biophysics· 1 Cell Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:cell type annotation· 2 Research Focus:cell-cell communication· 2 Research Focus:differential expression· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Organism:mouse· 2 Assay:proteomics· 2

Frequent Co-Authors

A. Martinson· 2 shared D. Bernstein· 2 shared D. Song· 2 shared F. Moussavi-Harami· 2 shared G. Flint· 2 shared J. A. Spudich· 2 shared J. Davis· 2 shared K. M. Ruppel· 2 shared

Activity by Year

2019-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersPhysiology

A. Martinson

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

PhysiologybioRxivPreprintJan 31, 2023

Danicamtiv increases myosin recruitment and alters the chemomechanical cross bridge cycle in cardiac muscle

K. B. Kooiker, S. Mohran, K. L. Turner…·F. Moussavi-Harami

This study investigates how Danicamtiv increases force and alters cardiac muscle contraction kinetics by modulating myosin function and cross bridge dynamics in cardiac tissue.

DOI 10.1101/2023.01.31.526380

mouseexperimental assay

𝕏 PostBluesky

Cell BiologybioRxivPreprintJan 23, 2023

Correcting dilated cardiomyopathy with fibroblast-targeted p38 deficiency

R. C. Bretherton, I. M. Reichardt, K. A. Zabrecky…·J. Davis

This study shows that targeting p38 in cardiac fibroblasts can reverse fibrosis and improve cardiomyocyte function in a mouse model of dilated cardiomyopathy.

DOI 10.1101/2023.01.23.523684

mouseexperimental assay

𝕏 PostBluesky

BiophysicsbioRxivPreprintNov 10, 2020

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…·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.

DOI 10.1101/2020.11.10.375493

humanproteomics

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BiochemistrybioRxivJan 31, 2019

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…·K. M. Ruppel

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

DOI 10.1038/s41467-019-10555-9

humanproteomics

𝕏 PostBluesky