Author

S. KOUNDRIOUKOFF

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· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Assay:DNA methylation· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

M. Debatisse· 3 shared A. Allouch· 1 shared A.-A. Muhammad· 1 shared A.-M. Lachages· 1 shared B. S. Lopez· 1 shared C. Maric· 1 shared C. Thermes· 1 shared C.-L. Chen· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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3 shared papersCancer Biology

M. Debatisse

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Palbociclib interferes with replication origin firing in a pRb independent manner

S.-J. Kim, C. Maric, l.-m. Briu, F. Fauchereau, G. Baldacci, M. Debatisse, S. KOUNDRIOUKOFF, J. C. cadoret

This paper shows palbociclib disrupts DNA replication in pRb-deficient cells by reducing origin firing and pre-initiation complex loading, leading to replicative stress and decreased cell viability.

bioRxiv · Sep 21, 2022 · PreprintCancer Biology

In vivo inactivation of RAD51-mediated homologous recombination leads to premature aging, but not to tumorigenesis

G. Matos-Rodrigues, V. Barroca, A.-A. Muhammad, A. Allouch, S. Koundrioukoff, D. Lewandowski, E. Despras, J. Guirouilh-Barbat, L. Frappart, P. Kannouche, P. Dupaigne, E. Le Cam, J.-L. Perfettini, P.-H. Romeo, M. Debatisse, , B. S. Lopez

This study shows that inactivating RAD51 in mice causes premature aging but not cancer, suggesting RAD51 is critical for progenitor cell homeostasis.

bioRxiv · Jan 17, 2022 · PreprintCancer Biology

Unscheduled origin building in S-phase upon tight CDK1 inhibition suppresses CFS instability

O. BRISON, S. Gnan, D. Azar, M. Schmidt, S. KOUNDRIOUKOFF, S. El-Hilali, Y. Jaszczyszyn, A.-M. Lachages, C. Thermes, C.-L. Chen, M. Debatisse

The paper shows that tight CDK1 inhibition during S-phase reduces CFS instability by promoting extra replication origins in under-replicated regions.

bioRxiv · Nov 19, 2020 · PreprintCell Biology