Author

Rosalie T. Zwiggelaar

Norwegian University of Science and TechnologyORCID 0000-0002-8355-9357Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Developmental Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Håvard T. LindholmiD· 2 shared John Arne DahliD· 2 shared Madeleine FosslieiD· 2 shared Mara Martín-AlonsoiD· 2 shared Menno J. OudhoffiD· 2 shared Naveen Parmar· 2 shared Alberto Díez-SáncheziD· 1 shared Bruce Vallance· 1 shared

Activity by Year

2020-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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2 shared papersDevelopmental Biology

Håvard T. LindholmORCID

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2 papers

Recent·Most cited

LSD1 represses a neonatal/reparative gene program in adult intestinal epithelium

Rosalie T. Zwiggelaar, Håvard T. Lindholm, Madeleine Fosslie, Marianne Terndrup Pedersen, Yuki Ohta, Alberto Díez-Sánchez, Mara Martín-Alonso, Jenny Ostrop, Mami Matano, Naveen Parmar, Emilie Kvaløy, Roos R. Spanjers, Kamran Nazmi, Morten Beck Rye, Finn Drabløs, , Menno J. Oudhoff

This study identifies LSD1 as a repressor of a neonatal/reparative gene program in adult intestinal epithelium, showing its role in Paneth cell differentiation and regenerative capacity.

Science Advances · Sep 11, 2020Peer-reviewedDevelopmental Biology

Intestinal-epithelial LSD1 controls cytoskeletal-mediated cell identity including goblet cell effector responses required for gut inflammatory and infectious diseases

Naveen Parmar, Kyle Burrows, Håvard T. Lindholm, Rosalie T. Zwiggelaar, Mara Martín-Alonso, Madeleine Fosslie, Bruce Vallance, John Arne Dahl, Colby Zaph, Menno J. Oudhoff

This study shows that intestinal-epithelial LSD1 deletion leads to increased pathogenesis in inflammatory and infectious disease models by impairing cytoskeletal organization and goblet cell effector responses.

bioRxiv · Jul 9, 2020Immunology