Author

Anna Sanchez Avila

University of Sheffield

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 Neuroscience· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:differential expression· 2 Approach:experimental assay· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:metagenomics· 1 Organism:mouse· 1

Frequent Co-Authors

Brittany C. S. Ellis· 2 shared Rachel E. HodgsoniD· 2 shared Sabin J. John· 2 shared Tatyana A. ShelkovnikovaiD· 2 shared Vedanth KumariD· 2 shared Wan-Ping HuangiD· 2 shared Adam K. WalkeriD· 1 shared Anna McFarlaneiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersCell Biology

Brittany C. S. Ellis

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Author profile →

3 papers

Recent·Most cited

Breakdown in the synaptic vesicle cycle defines early and reversible cortical pathogenesis in ALS

Zsófia I. László, Anna Sanchez Avila, Anna McFarlane, Dinja van der Hoorn, Rebecca San Gil, Tara L. Spires‐Jones, Thomas Henry Gillingwater, Adam K. Walker, Christopher M. Henstridge

The paper identifies early synaptic vesicle cycle disruption in ALS using proteomics and shows it is reversible with TDP-43 suppression.

bioRxiv · Aug 25, 2026 · PreprintNeuroscience

STMN2 protein depletion via translation deficits and stress granules and its compensation in ALS

Brittany C. S. Ellis, Anna Sanchez Avila, Wan-Ping Huang, Sabin J. John, Sam Bonsall, Rachel E. Hodgson, Vedanth Kumar, Matthew Nolan, Susan G. Campbell, Kurt J. De Vos, Clotilde Lagier‐Tourenne, J. Robin Highley, Johnathan Cooper‐Knock, Tatyana A. Shelkovnikova

This study identifies TDP-43-independent mechanisms of STMN2 depletion in ALS, showing acute stress causes proteasomal degradation and translational repression, while chronic stress leads to reduced protein levels, with mRNA upregulation as a compensatory mechanism in some subtypes.

bioRxiv · Jan 26, 2026 · PreprintCell Biology

FUS post-transcriptional splicing is autoregulated via RNA condensation with therapeutic potential for ALS-FUS

Wan-Ping Huang, Vedanth Kumar, Karen Yap, Haiyan An, Sabin J. John, Rachel E. Hodgson, Anna Sanchez Avila, Emily Day, Brittany C. S. Ellis, Tek Hong Chung, Jenny Lord, Michaela Müller-McNicoll, Eugene V. Makeyev, Tatyana A. Shelkovnikova

This study shows that FUS RNA condensation regulates its splicing and that disrupting this process can reduce FUS levels, offering a potential therapeutic strategy for ALS-FUS.

Science Advances · Jul 23, 2025Peer-reviewedCell Biology