A5032175334- DNA Repair Mechanisms
- CRISPR and Genetic Engineering
- PARP inhibition in cancer therapy
- Nuclear Structure and Function
- Adipokines, Inflammation, and Metabolic Diseases
- Cancer-related Molecular Pathways
- Carcinogens and Genotoxicity Assessment
- Genomics and Chromatin Dynamics
- BRCA gene mutations in cancer
- Genetics, Bioinformatics, and Biomedical Research
- Microtubule and mitosis dynamics
- Adipose Tissue and Metabolism
- DNA and Nucleic Acid Chemistry
- Cardiovascular Disease and Adiposity
- Cardiac Fibrosis and Remodeling
- RNA Research and Splicing
- RNA and protein synthesis mechanisms
- Cancer Research and Treatments
- Extracellular vesicles in disease
- Clay minerals and soil interactions
- Chromosomal and Genetic Variations
- Advanced biosensing and bioanalysis techniques
- RNA Interference and Gene Delivery
- Cancer therapeutics and mechanisms
- Bioinformatics and Genomic Networks
Centre National de la Recherche Scientifique
2016-2025
Inserm
2019-2025
Université Paris Cité
2019-2025
Institut Cochin
2012-2025
Central University Hospital of Asturias
2024
Thomas Jefferson University
2014-2024
Université Paris-Saclay
2014-2022
ORCID
2022
Institut Gustave Roussy
2012-2020
Biotherapy of Genetic Diseases, Inflammatory Disorders and Cancers
2012-2020
Research Article5 April 2011Open Access Down-regulation of BRCA1 expression by miR-146a and miR-146b-5p in triple negative sporadic breast cancers Amandine I. Garcia CNRS UMR5286 Inserm U1052, "Equipe Labellisée LIGUE 2008", University Lyon 1, Cancer Center Lyon, Centre Léon Bérard, France Search for more papers this author Monique Buisson Pascale Bertrand CNRS-CEA UMR 217, Institut de Radiobiologie Cellulaire et Moléculaire, Fontenay-aux-Roses, Ruth Rimokh Etienne Rouleau Laboratoire...
In genome editing with CRISPR-Cas9, transgene integration often remains challenging. Here, we present an approach for increasing the efficiency of by homology-dependent repair (HDR). CtIP, a key protein in early steps homologous recombination, is fused to Cas9 and stimulates HDR at human AAVS1 safe harbor locus. A minimal N-terminal fragment designated HE enhancer, sufficient stimulate this depends on CDK phosphorylation sites multimerization domain essential CtIP activity recombination....
XRCC4-null mice have a more severe phenotype than KU80-null mice. Here, we address whether this difference in is connected to nonhomologous end-joining (NHEJ). We used intrachromosomal substrates monitor NHEJ of two distal double-strand breaks (DSBs) targeted by I-SceI, living cells. In xrcc4-defective XR-1 cells, residual but significant process exists, which primarily uses microhomologies from the DSB. However, efficiency was strongly reduced cells versus complemented contrasting with...
Background: Diabetes mellitus exacerbates myocardial ischemia/reperfusion (MI/R) injury by incompletely understood mechanisms. Adipocyte dysfunction contributes to remote organ injury. However, the molecular mechanisms linking dysfunctional adipocytes increased MI/R remain unidentified. The current study attempted clarify whether and how small extracellular vesicles (sEV) may mediate pathological communication between diabetic cardiomyocytes, exacerbating Methods: Adult male mice were fed a...
DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein–interacting protein (CtIP) is phosphorylated in G2 cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating G1 unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates damage-inducible manner impacts on...
Homologous recombination plays a fundamental role in DNA double-strand break repair. Previously, we detected two mammalian nuclear proteins of 100 and 75 kDa (POMp100 POMp75, respectively) that are able to promote homologous pairing, key step recombination. Here describe the identification human (h) POMp75 as pro-oncoprotein TLS/FUS. hPOMp75/TLS binds both single- double-stranded DNAs mediates annealing complementary strands. More important, it promotes uptake single-stranded oligonucleotide...
Abstract AKT1 is frequently up-regulated in sporadic breast cancer, whereas BRCA1 mutated familial cancer. Because involved homologous recombination (HR), we addressed whether also has an effect on this process. We showed that repressed HR through cytoplasmic retention of and RAD51 proteins, resulting a BRCA1-deficient–like phenotype. This process does not require direct phosphorylation by AKT1. The correlated with activated tumor cell lines biopsies from cancers. Under nonpathologic...
The repair of toxic double-strand breaks (DSB) is critical for the maintenance genome integrity. major mechanisms that cope with DSB are: homologous recombination (HR) and classical or alternative nonhomologous end joining (C-NHEJ versus A-EJ). Because these pathways compete DSB, choice appropriate pathway pivotal. Among influence this choice, deoxyribonucleic acid (DNA) resection plays a role by driving cells to HR, while accurate C-NHEJ suppressed. Furthermore, promotes error-prone A-EJ....
Highlights•Nuclease-dependent DNA damage events are induced in Chk1-deficient cells•Activation of the ATM pathway limits precursors available for replication•DNA precursor starvation elicits replication fork slowing these cells•Origin firing is fine-tuned by speed independently Chk1 statusSummaryMammalian cells deficient ATR or display moderate and increased initiation density, but underlying mechanisms have remained unclear. We show that exogenous deoxyribonucleosides suppress both...
Significance Faithful genome duplication requires the precise coordination of DNA replication, repair/recombination and chromosome segregation. Homologous recombination (HR) plays a pivotal role in resumption blocked replication forks, HR − cells exhibit both spontaneous slower genome-wide fork speed mitotic extra centrosomes (MECs). We show that MECs result from slow kinetics are associated with multipolar mitosis leading to general unbalanced Thus, low levels stress, which not detected by...