Author

D. Durocher

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

Biology Disciplines

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Cancer Biology· 4 Cell Biology· 2 Biochemistry· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Organism:human· 7 Approach:genetic perturbation / CRISPR· 6 Research Focus:cancer & tumor microenvironment· 4 Research Focus:cell type annotation· 4 Research Focus:cell signaling & trafficking· 2 Research Focus:chromatin & epigenetic regulation· 2 Assay:DNA methylation· 2 Approach:experimental assay· 2

Frequent Co-Authors

A. Alvarez-Quilon· 3 shared H. Melo· 3 shared S. Adam· 3 shared S. E. Rossi· 3 shared A. Martin· 2 shared A. Veloso· 2 shared G. Martino· 2 shared J. Desjardins· 2 shared

Activity by Year

2019-2022 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersCancer Biology

A. Alvarez-Quilon

Mutual co-authors in cluster

Author profile →

8 papers

Recent·Most cited

Interaction with C21ORF2 controls the cellular functions of the NEK1 kinase

J. Rouse, M. Gregorczyk, G. Pastore, P. Lis, S. Lange, F. Lamoliatte, T. Macartney, R. Toth, F. Brown, J. Hastie, D. Durocher

This study identifies C21ORF2 as a regulatory subunit of NEK1, showing that their interaction is critical for NEK1 function and that mutations disrupt this interaction, linking it to disease.

bioRxiv · Aug 31, 2022 · PreprintBiochemistry

Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability

Y. Lu, T. Cho, S. Mukherjee, A. A. Malik, N. Gonzalez-Foutel, C. F. Suarez, D. Derovic, R. H. Oh, E. Langille, K. Al-Zahrani, Z. Lin, R. Tsai, V. Rotter, P. Ashton-Prolla, L. B. Chemes, , D. Schramek

This study uses CRISPR screens to identify factors regulating wild-type and mutant p53 stability, finding distinct regulators for different p53 mutants and their implications in cancer.

bioRxiv · Mar 13, 2022Cancer Biology

Global cellular response to chemical perturbation of PLK4 activity and abnormal centrosome number

J. M. Tkach, R. Philip, A. Sharma, J. Strecker, D. Durocher, L. Pelletier

The paper identifies TRIM37 as a key mediator of growth arrest after PLK4 inhibition and shows that growth arrest correlates with PLK4 activity rather than mitotic length or centrosome number.

bioRxiv · Jun 25, 2021Cell Biology

CCNE1 amplification is synthetic-lethal with PKMYT1 kinase inhibition

D. Gallo, J. T. F. Young, J. Fourtounis, G. Martino, A. Alvarez-Quilon, C. Bernier, N. M. Duffy, R. Papp, A. Roulston, R. Stocco, J. Szychowski, A. Veloso, H. Alam, P. S. Baruah, A. Bonneau Fortin, , D. Durocher

The paper identifies PKMYT1 as a therapeutic target for CCNE1-amplified cancers, showing that its inhibition leads to synthetic lethality and tumor regression in combination with gemcitabine.

bioRxiv · Apr 8, 2021Cancer Biology

The CIP2A-TOPBP1 complex safeguards chromosomal stability during mitosis

M. De Marco Zompit, C. Mooser, S. Adam, S. E. Rossi, A. Jeanrenaud, P.-A. Leimbacher, D. Fink, D. Durocher, M. Stucki

This study identifies CIP2A as a mitosis-specific protein that forms a complex with TOPBP1 to regulate DSB repair and chromosomal stability during mitosis.

bioRxiv · Feb 8, 2021Cell Biology

CIP2A is a prime synthetic-lethal target for BRCA-mutated cancers

S. Adam, S. E. Rossi, N. Moatti, M. De Marco Zompit, T. F. Ng, A. Alvarez-Quilon, J. Desjardins, V. Bhaskaran, G. Martino, D. Setiaputra, S. M. Noordermeer, T. K. Ohsumi, N. Hustedt, R. K. Szilard, N. Chaudhary, , D. Durocher

The paper identifies CIP2A as a synthetic-lethal target in BRCA-mutated cancers by showing its essential role in mitotic chromosome stability and its interaction with TOPBP1.

bioRxiv · Feb 8, 2021 · PreprintCancer Biology

FAM72A antagonizes UNG2 to promote mutagenic uracil repair during antibody maturation

Y. Feng, C. Li, J. Stewart, P. Barbulescu, N. Seija Desivo, A. Alvarez Quilon, R. Pezo, M. Perera, K. Chan, A. Tong, R. Mohamad-Ramshan, M. Berru, D. Nakib, G. Li, G. Kardar, , A. Martin

This study identifies FAM72A as a regulator of mutagenic uracil repair during antibody maturation by antagonizing UNG2 activity.

bioRxiv · Dec 23, 2020Immunology

A genetic map of the response to DNA damage in human cells

M. Olivieri, T. Cho, A. Alvarez-Quilon, K. Li, M. J. Schellenberg, M. Zimmermann, N. Hustedt, S. E. Rossi, S. Adam, H. Melo, A. M. Heijink, G. Sastre-Moreno, N. Moatti, R. Szilard, A. McEwan, , D. Durocher

The paper identifies 840 genes involved in the DNA damage response through CRISPR/Cas9 screens and highlights specific gene functions in DNA repair and toxicity mechanisms.

bioRxiv · Nov 18, 2019Cancer Biology