Author

M.-E. Harper

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 1 Pathology· 1 Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

C. Pileggi· 2 shared A. Atrih· 1 shared A. Beauvais· 1 shared A. Buchler· 1 shared A. Hagerman· 1 shared A. Tierney· 1 shared A.-A. Dumont· 1 shared B. L. Schneider· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersPhysiology

C. Pileggi

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

More than a ligand: PD-L1 promotes oncolytic virus infection via a metabolic shift that inhibits the type I interferon pathway.

J. Hodgins, J. Abou-Hamad, A. Hagerman, E. Yakubovich, C. Tanese De Souza, M. Marotel, A. Buchler, S. Fadel, M. Park, C. Fong-McMaster, M. J. F. Crupi, J. C. Bell, M.-E. Harper, B. Rotstein, R. Auer, , M. Ardolino

PD-L1 promotes oncolytic virus infection by inhibiting the type I interferon pathway through a metabolic shift involving enhanced glycolysis and lactate production.

bioRxiv · Aug 31, 2022 · PreprintCancer Biology

Cardiomyocyte-specific Srsf3 deletion reveals a mitochondrial regulatory role

A.-A. Dumont, L. Dumont, D. Zhou, H. Giguere, C. Pileggi, M.-E. Harper, D. P. Blondin, M. S. Scott, M. Auger-Messier

This study shows that deleting Srsf3 in cardiomyocytes leads to mitochondrial dysfunction, reduced survival, and cardiac remodeling in mice.

bioRxiv · Jul 3, 2020Physiology

A mouse model for spinal muscular atrophy provides insights into non-alcoholic fatty liver disease pathogenesis

M.-O. Deguise, C. Pileggi, A. Beauvais, A. Tierney, L. Chehade, Y. De Repentigny, J. Michaud, M. Llavero-Hurtado, D. Lamont, A. Atrih, T. M. Wishart, T. H. Gillingwater, B. L. Schneider, M.-E. Harper, S. H. Parson, R. Kothary

This paper uses a mouse model of spinal muscular atrophy to study non-alcoholic fatty liver disease, finding that it develops steatohepatitis and identifies molecular mechanisms involved.

bioRxiv · Apr 29, 2020 · PreprintPathology