Author

Ashton J. Curtis

University College LondonORCID 0009-0008-8320-0169Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Molecular Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2

Frequent Co-Authors

Jian Zhu· 2 shared Matthew G. GoldiD· 2 shared Christopher J. PennyiD· 1 shared Dorota StudniarczykiD· 1 shared Mark FarrantiD· 1 shared Timothy W. ChurchiD· 1 shared

Activity by Year

2023-2025 · peak 1/yr

Co-Author Collaboration Network

6 top collaborators · 12 mutual co-author links

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2 shared papersNeuroscience

Jian Zhu

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2 papers

Recent·Most cited

NeuroscienceJournal of NeurosciencePeer-reviewedOct 23, 2025

Widely used CaMKII regulatory segment mutations cause tight actinin binding and dendritic spine enlargement in unstimulated neurons

Ashton J. Curtis, Jian Zhu, Dorota Studniarczyk…·Matthew G. Gold

This study shows that CaMKII T305A/T306A mutations cause tight actinin binding and dendritic spine enlargement in unstimulated neurons, suggesting a structural role for CaMKII in LTP.

DOI 10.1523/jneurosci.0795-25.2025

experimental assay

𝕏 PostBluesky

Molecular BiologyeLifePeer-reviewedJul 25, 2023

Molecular basis of interactions between CaMKII and α-actinin-2 that underlie dendritic spine enlargement

Ashton J. Curtis, Jian Zhu, Christopher J. Penny, Matthew G. Gold

This study identifies how CaMKII and α-actinin-2 interactions drive dendritic spine enlargement during structural LTP by revealing molecular mechanisms and structural insights.

15 citations

experimental assay

𝕏 PostBluesky