Author

Christophe Sirac

Centre National de la Recherche ScientifiqueORCID 0000-0002-1183-4989Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Pathology· 3 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:mouse· 3 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Organism:human· 1 Assay:protein structure· 1

Frequent Co-Authors

Gemma Martinez-RivasiD· 3 shared Sébastien BenderiD· 3 shared Alessio LampisiD· 2 shared Arnaud JaccardiD· 2 shared Émilie PinaultiD· 2 shared Frank BridouxiD· 2 shared Gilles Roussine Codo· 2 shared Karolina Weronika ŚwiderskaiD· 2 shared

Activity by Year

2024-2025 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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3 shared papersPathology

Gemma Martinez-RivasORCID

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Author profile →

4 papers

Recent·Most cited

Preclinical characterization of AT-03, a novel Serum Amyloid P fusion protein that demonstrates pan-amyloid binding and removal

Christophe Sirac, Gilles Roussine Codo, Arnaud Jaccard, Sébastien Bender, Gemma Martinez-Rivas, Frank Bridoux, Marie Clavel, Camille Villesuzanne, Oussama Taoui, Claire Carrion, Gregory Bell, Spencer D. Guthrie, Suganya Selvarajah, Andrew Vick, Stephen J. Kennel, , Jonathan S. Wall

This paper characterizes AT-03, a novel fusion protein that binds and removes various amyloid types, showing therapeutic efficacy in a mouse model.

bioRxiv · Dec 25, 2025 · PreprintPathology

Accelerated Apolipoprotein A-II senile amyloidosis in a PAI-1 (plasminogen activator inhibitor 1) knock-out model

Gilles Roussine Codo, Pauline Duchatelet, Gemma Martinez-Rivas, Alessio Lampis, Karolina Weronika Świderska, Émilie Pinault, Camille Cohen, Magali Colombat, Sébastien Bender, Christophe Sirac

This study shows PAI-1 knockout mice develop systemic AApoA-II amyloidosis at intermediate age, with amyloid deposits in multiple organs and urinary albumin as a biomarker, highlighting potential risks of PAI-1 inhibition in amyloidosis.

bioRxiv · Dec 23, 2025 · PreprintPathology

A mouse model of cardiac AL amyloidosis unveils mechanisms of tissue accumulation and toxicity of amyloid fibrils

Gemma Martinez-Rivas, Maria Victoria Ayala, Sébastien Bender, Gilles Roussine Codo, Karolina Weronika Świderska, Alessio Lampis, Laura Pedroza, Melisa Merdanovic, Pierre Sicard, Émilie Pinault, Laurence Richard, Francesca Lavatelli, Sofia Giorgetti, Diana Canetti, Alexa Rinsant, , Christophe Sirac

This paper develops a mouse model of cardiac AL amyloidosis that reproduces human disease features, including amyloid deposits and cardiac dysfunction, and identifies a role for partial LC degradation in fibril formation.

Nature Communications · Mar 27, 2025Peer-reviewedPathology

Selective killing of plasma cell clones using splice-switching oligonucleotides targeting immunoglobulin variable exons.

Jean-Marie Lambert, Antoine Praité, Marion Contini, Mohamad Omar Ashi, Anne Marchalot, Soazig Le Pennec, Christophe Sirac, Sandy Al Hayek, Laurent Delpy

This study shows that splice-switching ASOs targeting V exons in myeloma cells induce selective plasma cell clone death via ER stress and apoptosis.

bioRxiv · Aug 30, 2024 · PreprintImmunology