Author

D. Maggiorani

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

Cell Biology· 3 Cancer Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 4 Organism:human· 4 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Approach:statistical model· 2 Research Focus:differential expression· 1

Frequent Co-Authors

C. Beausejour· 3 shared A. Deprez· 1 shared A. Lagnado· 1 shared A. Parini· 1 shared A. Walaszczyk· 1 shared B. Benabdalah· 1 shared B. Benabdallah· 1 shared B. Ellezam· 1 shared

Activity by Year

2018-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 15 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

3 shared papersCell Biology

C. Beausejour

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Nuclear Location Bias of HCAR1 Drives Cancer Malignancy through Numerous Routes

M. A. M. Nezhady, G. Cagnone, E. Bajon, P. Chaudhari, M. Modaresinejad, P. Hardy, D. Maggiorani, C. Quiniou, J.-S. Joyal, C. Beausejour, S. Chemtob

This study identifies nuclear localization of HCAR1 as a driver of cancer malignancy through multiple mechanisms including nuclear signaling and transcriptomic regulation.

bioRxiv · Jul 25, 2022 · PreprintCell Biology

Clearance of defective muscle stem cells by senolytics reduces the expression of senescence-associated secretory phenotype and restores myogenesis in myotonic dystrophy type 1.

T. Conte, G. D. Bishop, Z. Orfi, I. Mokhtari, A. Deprez, M.-P. Roussel, I. Cote, O. Pellerito, D. Maggiorani, B. Benabdallah, S. Leclerc, L. Feulner, J. Mathieu, C. Gagnon, G. Andelfinger, , N. Dumont

This study identifies a senescent molecular signature in DM1 myogenic cells and shows that senolytics reduce SASP and restore myogenesis.

bioRxiv · Jun 22, 2022 · PreprintCell Biology

Autologous humanized mouse models of iPSC-derived tumors allow for the evaluation and modulation of cancer-immune cell interactions

G. Moquin-Beaudry, B. Benabdalah, D. Maggiorani, O. Le, Y. Li, C. Colas, C. Raggi, B. Ellezam, M. M'Callum, D. Dal Soglio, J. V. Guimond, M. Paganelli, E. Haddad, C. Beausejour

This paper develops autologous humanized mouse models of iPSC-derived tumors to study and modulate cancer-immune interactions, showing immune infiltration and response to PD-1 inhibition.

bioRxiv · Apr 2, 2021Cancer Biology

Length-independent telomere damage drives cardiomyocyte senescence

R. Anderson, A. Lagnado, D. Maggiorani, A. Walaszczyk, E. Dookun, J. Chapman, J. Birch, H. Salmonowicz, M. Ogrodnik, D. Jurk, C. Proctor, C. Correia-Melo, S. Victorelli, E. Fielder, R. Berlinguer-Palmini, , J. F. Passos

This study shows that telomere damage independent of length causes cardiomyocyte senescence, leading to cardiac dysfunction, and that clearing senescent cells improves cardiac health.

bioRxiv · Aug 17, 2018Cell Biology