Author

Emily Relton

The Pirbright Institute

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· 1 Genetics· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

Nicolas LockeriD· 2 shared Abuzar Kaleem· 1 shared Adam Hunter· 1 shared Alexandra S. NeaversoniD· 1 shared Andrew Day· 1 shared Andrew H. CrosbyiD· 1 shared Andrew Y. ShueniD· 1 shared Binnaz YalciniD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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2 shared papersCell Biology

Nicolas LockerORCID

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Author profile →

3 papers

Recent·Most cited

Capillary-based Subcellular Sampling Uncovers the Stress Granule Proteome in Single Cells

Claire Davison, Nicolas Locker, Mariana Marques, Sam Kelly, Emily Relton, Tanavi Sharma, Emily Fraser, Pedro Aragon-Fernandez, Erwin M. Schoof, Mia Petersen, Jordan Pascoe, Kathryn Susan Lilley, Sneha M. Pinto, Matt Spick, Melanie Jane Bailey

The paper introduces a capillary-based subcellular sampling method combined with LC-MS to analyze stress granule proteomes in single cells, identifying 405 high-confidence proteins with minimal cytosolic contamination.

bioRxiv · May 13, 2026 · PreprintCell Biology

The Batten disease protein CLN3 is important for stress granules dynamics and translational activity.

Emily Relton, Nicolas J. Roth, Seda Yaşa, Abuzar Kaleem, Guido Hermey, Christopher J. Minnis, Sara Mole, Tatyana A. Shelkovnikova, Stéphane Lefrançois, Peter James McCormick, Nicolas Locker

This study shows that CLN3 deficiency disrupts stress granule dynamics and translation, linking it to neurodegenerative disease mechanisms.

Journal of Biological Chemistry · Mar 23, 2023Peer-reviewedMolecular Biology

Mouse and cellular models of KPTN-related disorder implicate mTOR signalling in cognitive and progressive overgrowth phenotypes

Maria O. Levitin, Lettie E. Rawlins, Gabriela Sánchez-Andrade, Osama A. Arshad, Stephan C. Collins, Stephen J. Sawiak, Philip H. Iffland, Malin H. L. Andersson, Caleb P. Bupp, Emma L. Cambridge, Eve L. Coomber, Ian Ellis, Johanna C. Herkert, Holly Ironfield, Logan Jory, , Sebastian S. Gerety

The paper investigates KPTN-related disorder using mouse and human stem cell models, identifying mTOR pathway dysregulation as a key mechanism underlying cognitive and overgrowth phenotypes.

bioRxiv · Jul 15, 2022 · PreprintGenetics