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El Bachir Affar

Affar, El Bachir

Full professor


Université de Montréal

Research Axes


Contact information

Phone: 514-252-3400, poste3343


  • Diana Adjaoud
  • Oumaima Ahmed
  • Benjamin Estavoyer
  • Louis Masclef
  • Clémence Messmer
  • Maxime Uriarte

With a PhD in physiology and endocrinology, El Bachir Affar heads the Cell Signalling and Cancer Research Unit at Hôpital Maisonneuve-Rosemont. He is also a full professor in the Faculty of Medicine and an adjunct professor in the Department of Biochemistry and Molecular Medicine at Université de Montréal. 

El Bachir Affar is interested in cellular signalling via ubiquitination, DNA- and chromatin-dependent processes (DNA transcription and repair), and the molecular bases of cancer. His team works in particular on the BAP1 gene, which frequently mutates in some types of cancers.

Research Unit

Cellular Signalling and Cancer

Ubiquitination is a post-translational modification that plays a key role in regulating a number of cellular functions. Clinically speaking, the mutations of many genes in the ubiquitin system have been causally linked to various diseases, including cancer.  Ubiquitination is a reversible process due to the presence of deubiquitinating enzymes, or enzymes that specifically remove ubiquitin from target proteins. Although deubiquitinating enzymes are not well understood, they are nevertheless emerging as central regulators in the ubiquitin system. 

Our goal is to characterize the biological functions and mechanisms of action of the deubiquitinating enzymes involved in DNA transcription and repair, two processes whose deregulation plays a key role in the development of cancer.

We use state-of-the-art biochemistry, molecular biology, and cell culture approaches to characterize the functions of deubiquitinating enzymes. Our work provides a better understanding of the molecular mechanisms governing the ubiquitin system. New concepts may also be developed with regard to the regulation of DNA transcription and repair.

Our work should also help identify new therapeutic targets to treat cancer with personalized medicine.

  • Polycomb group-mediated histone H2A monoubiquitination in epigenome regulation and nuclear processes. Barbour H, Daou S, Hendzel M, Affar EB. Nat Commun. 2020 Nov 23;11(1):5947. doi: 10.1038/s41467-020-19722-9.
  • Roles and mechanisms of BAP1 deubiquitinase in tumor suppression. Masclef L, Ahmed O, Estavoyer B, Larrivée B, Labrecque N, Nijnik A, Affar EB. Cell Death Differ. 2021 Feb;28(2):606-625. doi: 10.1038/s41418-020-00709-4. Epub 2021 Jan 18.
  • Monoubiquitination of ASXLs controls the deubiquitinase activity of the tumor suppressor BAP1.Daou S, Barbour H, Ahmed O, Masclef L, Baril C, Sen Nkwe N, Tchelougou D, Uriarte M, Bonneil E, Ceccarelli D, Mashtalir N, Tanji M, Masson JY, Thibault P, Sicheri F, Yang H, Carbone M, Therrien M, Affar EB. Nat Commun. 2018 Oct 22;9(1):4385. doi: 10.1038/s41467-018-06854-2
  • USP42 deubiquitinase in the arena of liquid-liquid phase separation and nuclear speckles. Uriarte M, Milot E, Affar EB. Cell Death Differ. 2021 Jun;28(6):2022-2024. doi: 10.1038/s41418-021-00794-z. Epub 2021 May 10.
  • A potent nuclear export mechanism imposes USP16 cytoplasmic localization during interphase. Sen Nkwe N, Daou S, Uriarte M, Gagnon J, Iannantuono NV, Barbour H, Yu H, Masclef L, Fernández E, Zamorano Cuervo N, Mashtalir N, Binan L, Sergeev M, Bélanger F, Drobetsky E, Milot E, Wurtele H, Costantino S, Affar EB. J Cell Sci. 2020 Feb 24;133(4):jcs239236. doi: 10.1242/jcs.239236.
  • BAP1 regulates different mechanisms of cell death. Affar EB, Carbone M. Cell Death Dis. 2018 Nov 19;9(12):1151. doi: 10.1038/s41419-018-1206-5.
  • BAP1 regulates IP3R3-mediated Ca2+ flux to mitochondria suppressing cell transformation. Bononi A, Giorgi C, Patergnani S, Larson D, Verbruggen K, Tanji M, Pellegrini L, Signorato V, Olivetto F, Pastorino S, Nasu M, Napolitano A, Gaudino G, Morris P, Sakamoto G, Ferris LK, Danese A, Raimondi A, Tacchetti C, Kuchay S, Pass HI, Affar EB, Yang H, Pinton P, Carbone M. Nature. 2017 Jun 22;546(7659):549-553.
  • The BAP1/ASXL2 Histone H2A Deubiquitinase Complex Regulates Cell Proliferation and Is Disrupted in Cancer. Daou S, Hammond-Martel I, Mashtalir N, Barbour H, Gagnon J, Iannantuono NV, Nkwe NS, Motorina A, Pak H, Yu H, Wurtele H, Milot E, Mallette FA, Carbone M, Affar el B .J Biol Chem. 2015 Nov 27;290(48):28643-63.
  • Undetectable histone O-GlcNAcylation in mammalian cells. Gagnon J, Daou S, Zamorano N, Iannantuono NV, Hammond-Martel I, Mashtalir N, Bonneil E, Wurtele H, Thibault P, Affar el B. Epigenetics. 2015;10(8):677-91.
  • Autodeubiquitination protects the tumor suppressor BAP1 from cytoplasmic sequestration mediated by the atypical ubiquitin ligase UBE2O. Mashtalir N, Daou S, Barbour H, Sen NN, Gagnon J, Hammond-Martel I, Dar HH, Therrien M, Affar el B. Mol Cell. 2014 May 8;54(3):392-406.
  • Tumor suppressor and deubiquitinase BAP1 promotes DNA double-strand break repair. Yu H, Pak H, Hammond-Martel I, Ghram M, Rodrigue A, Daou S, Barbour H, Corbeil L, Hébert J, Drobetsky E, Masson JY, Di Noia JM, Affar el B. Proc Natl Acad Sci U S A. 2014 Jan 7;111(1):285-90.


  • Postdoctoral fellowship

    Department of Pathology, Harvard Medical School, Boston

  • Postdoctoral fellowship

    Skin Cancer Research Laboratory, Centre hospitalier de l'Université Laval (CHUL), Québec City

  • PhD in physiology and endocrinology

    Centre hospitalier de l'Université Laval (CHUL), Québec City


  • 2016 Senior Research Scholar (FRQS)
  • 2011 New Investigator Award (CIHR)
  • 2011 Junior 2 Research Scholar (FRQS)
  • 2011 Finalist for the Maud Menten New Principal Investigator Prize (Institute of Genetics, CIHR)
  • 2007 Junior 1 Research Scholar (FRQS)
  • 2001 Taplin Postdoctoral Fellowship (Harvard University, Boston)
  • 1999 Dean’s Honour List – PhD (Université Laval)
  • 1991 Award of excellence for graduate studies (Ministry of National Education, Morocco)