Author

E. Meredith

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· 4

Signature Assays, Organisms & Methods

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Organism:human· 4 Approach:genetic perturbation / CRISPR· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Research Focus:cell-cell communication· 2 Research Focus:differential expression· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

J. T. Hinson· 2 shared K. Thakar· 2 shared R. Cohn· 2 shared Y.-s. Chen· 2 shared A. Lowe· 1 shared A. M. Pettinato· 1 shared A. Pettinato· 1 shared A. W. Orr· 1 shared

Activity by Year

2018-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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2 shared papersCell Biology

J. T. Hinson

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Author profile →

4 papers

Recent·Most cited

CD13 Activation Assembles Signaling Complexes that Promote the Formation of Tunneling Nanotubes in Endothelial Cells

E. Meredith, B. Aguilera, F. McGurk, P. Zong, L. Yue, L. H. Shapiro, M. Ghosh

This study shows CD13 activates signaling complexes that promote TNT formation in endothelial cells by regulating PI signaling and actin dynamics.

bioRxiv · May 10, 2024 · PreprintCell Biology

Gamma protocadherins in vascular endothelial cells inhibit Klf2/4 to promote atherosclerosis

D. Joshi, B. G. Coon, R. Chakraborty, H. Deng, P. Fernandez Tussy, E. Meredith, J. G. Traylor, A. W. Orr, C. Fernandez-Hernando, M. A. Schwartz

This study identifies Pcdhg as a suppressor of Klf2/4 in endothelial cells, promoting atherosclerosis by inhibiting the Notch pathway.

bioRxiv · Jan 16, 2024 · PreprintCell Biology

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