Author

Frédéric Bard

Agency for Science, Technology and ResearchORCID 0000-0002-3783-4805Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 1 Cell Biology· 1 Genetic & Genomic Medicine· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Organism:mouse· 2 Assay:proteomics· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Xavier Le GuezenneciD· 2 shared Abigail LohiD· 1 shared Afaf Alsubhi· 1 shared Aida Maria Bertoli‐AvellaiD· 1 shared Ajay Sriram MathuruiD· 1 shared Alex ChauviniD· 1 shared Anh Tuan NguyeniD· 1 shared Arda ÇetinkayaiD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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2 shared papersCancer Biology

Xavier Le GuezennecORCID

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Author profile →

3 papers

Recent·Most cited

Co-translational O-glycosylation driven by GALNTs spatial reprogramming fosters pancreatic cancer growth

Rebecca Bennion, Eugénie Lohmann, Giacomo Del Rio, Lucile Rouyer, Sahar El Amrani, Małgorzata Kowalczewska, Xavier Le Guezennec, Eric Mas, Nelson Dusetti, Alex Chauvin, Richard Tomasini, Sophie Vasseur, Fabienne Guillaumond, Brice Chanez, Martin James Humphries, , Frédéric Bard

The paper shows that GALA, a process relocating GALNTs to the ER, enables co-translational O-glycosylation in pancreatic cancer, expanding the O-glycoproteome and promoting tumor growth.

bioRxiv · Sep 8, 2026 · PreprintCancer Biology

ER O-glycosylation in synovial fibroblasts drives cartilage degradation

Le Son Tran, Joanne Chia, Xavier Le Guezennec, Keit Min Tham, Anh Tuan Nguyen, Virginie Sandrin, Way Cherng Chen, Tan Tong Leng, Sreedharan Sechachalam, Khai Pang Leong, Frédéric Bard

This study identifies ER O-glycosylation by GALNTs in synovial fibroblasts as a driver of cartilage degradation in arthritis, with Calnexin as a potential therapeutic target.

Nature Communications · Mar 14, 2025Peer-reviewedCell Biology

Loss of C2orf69 defines a fatal auto-inflammatory mitochondriopathy in Humans and Zebrafish

Hui Hui Wong, Sze Hwee Seet, Michael Maier, Ayse Gurel, Ricardo Moreno Traspas, Cheryl Q. E. Lee, Shan Zhang, Beril Talim, Abigail Loh, Crystal Y. Chia, Tze Shin Teoh, Danielle Sng, Jarred W. Rensvold, Şule Ünal, Evgenia Shishkova, , Bruno Reversade

The paper identifies C2orf69 deficiency as a cause of a fatal auto-inflammatory syndrome in humans and zebrafish, affecting mitochondrial function and immune/cNS development.

The American Journal of Human Genetics · May 25, 2021Peer-reviewedGenetic & Genomic Medicine