Author

E. Moeendarbary

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 Bioengineering· 1

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 2 Approach:mechanistic / dynamical model· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:development & morphogenesis· 1 Approach:experimental assay· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Assay:imaging· 1

Frequent Co-Authors

F. Spill· 2 shared J. Escribano· 2 shared J. M. Garcia-Aznar· 2 shared A. T. Weeraratna· 1 shared E. McEvoy· 1 shared G. Charras· 1 shared G. E. Marino· 1 shared L. I. Korsak· 1 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersBiophysics

F. Spill

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The cytoplasm of living cells can sustain transient and steady intracellular pressure gradients

M. Malboubi, M. H. Esteki, M. B. Vaghela, L. I. Korsak, R. J. Petrie, E. Moeendarbary, G. Charras

This study shows that cells can sustain intracellular pressure gradients over minutes, revealing the role of cytoplasmic poroelasticity in mechanical responses and cell physiology.

bioRxiv · Apr 22, 2024Biophysics

Modeling the three-way feedback between cellular contractility, actin polymerization, and adhesion turnover resolves the contradictory effects of RhoA and Rac1 on endothelial junction dynamics

E. McEvoy, T. Sneh, E. Moeendarbary, G. E. Marino, X. Chen, J. Escribano, F. Spill, J. M. Garcia-Aznar, A. T. Weeraratna, T. M. Svitkina, R. D. Kamm, V. B. Shenoy

This study develops a chemo-mechanical model to explain how RhoA and Rac1 differentially affect endothelial junction dynamics through their roles in contractility, adhesion turnover, and actin polymerization.

bioRxiv · Mar 15, 2021 · PreprintBiophysics

Balance of Mechanical Forces Drives Endothelial Gap Formation and May Facilitate Cancer and Immune-Cell Extravasation

J. Escribano, M. Chen, E. Moeendarbary, X. Cao, V. Shenoy, J. M. Garcia-Aznar, R. Kamm, F. Spill

This study shows that mechanical forces drive spontaneous gap formation in endothelial cells, which may facilitate cancer and immune cell extravasation by preferentially occurring at cell vertices.

bioRxiv · Nov 26, 2018Bioengineering