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Bernard S. Lopez

Researcher at Centre national de la recherche scientifique

Publications -  65
Citations -  4646

Bernard S. Lopez is an academic researcher from Centre national de la recherche scientifique. The author has contributed to research in topics: Homologous recombination & DNA repair. The author has an hindex of 36, co-authored 61 publications receiving 4366 citations. Previous affiliations of Bernard S. Lopez include University of Paris-Sud & Curie Institute.

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Characterization of homologous recombination induced by replication inhibition in mammalian cells

TL;DR: It is proposed that replication inhibition produces DSBs, which are first processed by the NHEJ; then, following DSB accumulation, RAD51 recombination can act.
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Impact of the KU80 Pathway on NHEJ-Induced Genome Rearrangements in Mammalian Cells

TL;DR: Using a substrate measuring deletion or inversion of an I-SceI-excised fragment and both accurate and inaccurate rejoining, the impact of non-homologous end-joining (NHEJ) on mammalian chromosome rearrangements is determined and these processes should represent prominent pathways for DSB-induced genetic instability in mammalian cells.
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Role of Mre11 in chromosomal nonhomologous end joining in mammalian cells

TL;DR: It is shown that, in addition to its role in ATM activation, Mre11 can favor alternative NHEJ through its nuclease activity, as well as affecting both the canonical and alternative pathways.
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Down-regulation of BRCA1 Expression by miR-146a and miR-146b-5p in Triple Negative Sporadic Breast Cancers

TL;DR: This work provides further evidence for the involvement of miRNAs in sporadic breast cancer through down‐regulation of BRCA1 through binding to the same site in the 3′UTR of BrcA1 and down‐regulate its expression as demonstrated using reporter assays.
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Oxidative stress induces an ATM‐independent senescence pathway through p38 MAPK‐mediated lamin B1 accumulation

TL;DR: Data reveal lamin B1 as a general molecular mediator that controls OS‐induced senescence, independent of established Ataxia Telangiectasia Mutated (ATM) roles in OIS.