Author

Sean Ahmadi

University of Virginia

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 Developmental Biology· 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 Assay:proteomics· 1

Frequent Co-Authors

David L. BrautiganiD· 2 shared Wenhao XuiD· 2 shared Zheng FuiD· 2 shared Ana Limerick· 1 shared Casey D. GaileyiD· 1 shared Cheuk Ying Chu· 1 shared Ellie A. McCabe· 1 shared Eric J. Wang· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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2 shared papersCell Biology

David L. BrautiganORCID

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2 papers

Recent·Most cited

An epilepsy-associated CILK1 variant compromises KATNIP regulation and impairs primary cilia and Hedgehog signaling

Ana Limerick, Ellie A. McCabe, Jacob S. Turner, Kevin W. Kuang, David L. Brautigan, Yi Hao, Cheuk Ying Chu, Sean H. Fu, Sean Ahmadi, Wenhao Xu, Zheng Fu

This study shows that a CILK1 variant linked to epilepsy impairs primary cilia and Hedgehog signaling by disrupting KATNIP regulation in mouse cells.

Cells · Jul 26, 2024Peer-reviewedCell Biology

Phosphosite T674A mutation in kinesin family member 3A fails to reproduce tissue and ciliary defects characteristic of CILK1 loss of function

Casey D. Gailey, Eric J. Wang, Li Jin, Sean Ahmadi, David L. Brautigan, Xudong Joshua Li, Wenhao Xu, Michael M. Scott, Zheng Fu

The paper shows that mutating KIF3A's phosphorylation site T674 to Ala in mice does not reproduce the severe ciliopathy defects seen with CILK1 loss of function.

Developmental Dynamics · Sep 16, 2020Peer-reviewedDevelopmental Biology