Author

B. Stott

University of Oxford

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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Molecular Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

C. Duarte· 2 shared A. K. Wann· 1 shared Angus K. T. WanniD· 1 shared C. R. Coveney· 1 shared Clarissa R. CoveneyiD· 1 shared E. Chang· 1 shared Eleanor McSorley· 1 shared Emer ChangiD· 1 shared

Activity by Year

2021-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersPhysiology

C. Duarte

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2 papers

Recent·Most cited

Ciliary IFT88 safeguards coordinated epiphyseal vascularisation, resorption and ossification from disruptive physiological mechanical forces

C. R. Coveney, J. Samvelyan, J. Miotla-Zarebska, J. Carnegie, E. Chang, J. Corrin, T. Coveney, B. Stott, I. Parisi, C. Duarte, T. L. Vincent, K. A. Staines, A. K. Wann

This study shows that IFT88 in cilia protects growth plate ossification from mechanical forces by regulating vascularization and resorption in adolescent mice.

bioRxiv · Aug 6, 2021 · PreprintPhysiology

The ciliary protein IFT88 controls post-natal cartilage thickness and influences development of osteoarthritis.

Clarissa R. Coveney, Linyi Zhu, Jadwiga Miotla‐Zarebska, B. Stott, Ida Parisi, Vicky Batchelor, C. Duarte, Emer Chang, Eleanor McSorley, Tonia L. Vincent, Angus K. T. Wann

This study shows that IFT88 deletion leads to reduced cartilage thickness and increased osteoarthritis in mice, with exercise partially reversing these effects.

Arthritis & Rheumatology · Jun 9, 2021Peer-reviewedMolecular Biology