Author

Edward L. Hurley

University at Buffalo, State University of New YorkORCID 0000-0002-1967-8933Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Emma R. WilsoniD· 3 shared Lawrence G. WrabetziD· 3 shared M. Laura FeltriiD· 3 shared Gustavo Della‐Flora NunesiD· 2 shared Yannick PoiteloniD· 2 shared Alexander Martin RossoriD· 1 shared Bert W. O’MalleyiD· 1 shared Bin HeiD· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersNeuroscience

Emma R. WilsonORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Loss of prohibitin 2 in Schwann cells dysregulates key transcription factors controlling developmental myelination

Emma R. Wilson, Gustavo Della‐Flora Nunes, Shichen Shen, Seth M. Moore, Joseph M Gawron, Jessica Maxwell, Umair Syed, Edward L. Hurley, Meghana Lanka, Jun Qu, Laurent Désaubry, Lawrence G. Wrabetz, Yannick Poitelon, M. Laura Feltri

This study shows that loss of Phb2 in Schwann cells disrupts myelination and dysregulates key transcription factors essential for peripheral nerve development.

Glia · Aug 31, 2024Peer-reviewedNeuroscience

MPZ-T124M mouse model replicates human axonopathy and suggest alteration in axo-glia communication

Ghjuvan’Ghjacumu Shackleford, Leandro N. Marziali, Yo Sasaki, Nadav I. Weinstock, Alexander Martin Rossor, Nicholas J. Silvestri, Emma R. Wilson, Edward L. Hurley, Grahame J. Kidd, Senthilvelan Manohar, Dalian Ding, Richard Salvi, M. Laura Feltri, Maurizio D’Antonio, Lawrence G. Wrabetz

The paper develops a P0T124M mouse model of CMT2J neuropathy, showing axonal damage without significant myelin defects and altered axo-glia communication.

bioRxiv · May 9, 2022 · PreprintNeuroscience

mTORC1 and JUN are activated after deletion of Prohibitin 1 in Schwann cells and may link mitochondrial dysfunction to demyelination

Gustavo Della‐Flora Nunes, Emma R. Wilson, Edward L. Hurley, Bin He, Bert W. O’Malley, Yannick Poitelon, Lawrence G. Wrabetz, M. Laura Feltri

This study shows that mTORC1 and JUN are activated in Schwann cells lacking Prohibitin 1, contributing to demyelination through mitochondrial dysfunction.

eLife · Sep 14, 2021Peer-reviewedNeuroscience