Author

Manu Ahmed

University of Massachusetts Chan Medical SchoolORCID 0000-0002-2841-1624Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 2

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Research Focus:development & morphogenesis· 2 Approach:experimental assay· 2 Organism:mouse· 2 Organism:C. elegans· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

Karyn L. RobertiD· 2 shared Sumeda NandadasaiD· 2 shared Colin A. JohnsoniD· 1 shared Gregory J. PazouriD· 1 shared Griffin I. KaneiD· 1 shared Karen I. LangeiD· 1 shared Matthew A. KavanaughiD· 1 shared Michael W. StuckiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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2 shared papersCell Biology

Karyn L. RobertORCID

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2 papers

Recent·Most cited

Loss of ADAMTS9 disrupts ciliogenesis and collagen homeostasis resulting in Nephronophthisis-like polycystic kidneys

Sydney Fischer, Karyn L. Robert, Manu Ahmed, Griffin I. Kane, Matthew A. Kavanaugh, Wei Wang, Pamela Vivian Tran, Prabhani U. Atukorale, Sumeda Nandadasa

This study shows ADAMTS9 deletion in mice causes polycystic kidney disease by disrupting ciliogenesis and collagen homeostasis, leading to small, cystic kidneys and early lethality in males.

JCI Insight · Sep 24, 2026Peer-reviewedCell Biology

Two functional forms of the Meckel-Gruber syndrome protein TMEM67 generated by proteolytic cleavage by ADAMTS9 mediate Wnt signaling and ciliogenesis

Manu Ahmed, Sydney Fischer, Karyn L. Robert, Karen I. Lange, Michael W. Stuck, Sunayna K. Best, Colin A. Johnson, Gregory J. Pazour, Oliver E. Blacque, Sumeda Nandadasa

Nature Communications · May 28, 2025Peer-reviewedCell Biology