Author

E. Bennett

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Approach:biophysical modeling· 1 Organism:yeast· 1

Frequent Co-Authors

A. Fulzele· 1 shared A. M. Day· 1 shared D. Byrne· 1 shared E. A. Veal· 1 shared E. Dwyer· 1 shared E. HUI· 1 shared G. Fu· 1 shared H. R. Latimer· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCell Biology

A. Fulzele

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2 papers

Recent·Most cited

A Peroxiredoxin-P38 MAPK scaffold increases MAPK activity by MAP3K-independent mechanisms

M. Cao, A. M. Day, M. Galler, H. R. Latimer, D. Byrne, E. Bennett, E. Dwyer, P. A. Eyers, E. A. Veal

This paper shows that a Peroxiredoxin-P38 MAPK fusion protein hyperactivates P38 MAPK in yeast and human cells without requiring H2O2-sensing cysteines, suggesting a novel scaffold-based signaling mechanism.

bioRxiv · Nov 15, 2022Biochemistry

BTLA and PD-1 employ distinct phosphatases to differentially repress T cell signaling

X. Xu, A. Fulzele, Y. Zhao, Z. Wu, Y. Hu, Y. Jiang, Y. Ma, H. Wang, G. Fu, E. Bennett, E. HUI

This study identifies that BTLA and PD-1 use distinct phosphatases to differentially repress T cell signaling, highlighting mechanistic differences between two co-inhibitory receptors.

bioRxiv · Jun 14, 2019Cell Biology