Author

K. Thakar

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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Cell Biology· 2

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Approach:genetic perturbation / CRISPR· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Assay:proteomics· 1

Frequent Co-Authors

E. Meredith· 2 shared J. T. Hinson· 2 shared R. Cohn· 2 shared Y.-s. Chen· 2 shared A. Lowe· 1 shared A. M. Pettinato· 1 shared A. Pettinato· 1 shared B. Huey· 1 shared

Activity by Year

2018-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersCell Biology

E. Meredith

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2 papers

Recent·Most cited

Identifying cardiac actinin interactomes reveals sarcomere crosstalk with RNA-binding proteins

F. A. Ladha, K. Thakar, A. M. Pettinato, N. Legere, R. Cohn, R. Romano, E. Meredith, Y.-s. Chen, J. T. Hinson

The paper identifies cardiac actinin interactomes, revealing sarcomere crosstalk with RNA-binding proteins like IGF2BP2 that affect mitochondrial function and sarcomere assembly.

bioRxiv · Mar 18, 2020Cell Biology

A contraction stress model of hypertrophic cardiomyopathy due to thick filament sarcomere mutations

R. Cohn, K. Thakar, A. Lowe, F. Ladha, A. Pettinato, E. Meredith, Y.-s. Chen, K. Atamanuk, B. Huey, J. T. Hinson

This study uses CRISPR/Cas9 to create HCM iPSc models and finds that mutations cause hypercontractility and p53 activation linked to oxidative stress, suggesting p53 as a therapeutic target.

bioRxiv · Sep 4, 2018Cell Biology