Thibaut Peterlini

ORCID: 0009-0003-6932-0432
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About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • CRISPR and Genetic Engineering
  • PARP inhibition in cancer therapy
  • Cancer therapeutics and mechanisms
  • Plant Genetic and Mutation Studies
  • Microtubule and mitosis dynamics
  • Biomedical Ethics and Regulation
  • Carcinogens and Genotoxicity Assessment
  • Heat shock proteins research
  • Pluripotent Stem Cells Research
  • BRCA gene mutations in cancer
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research

Université Laval
2018-2023

Quebec Research and Development Centre
2021

Centre hospitalier universitaire de Québec
2021

Cancer Research Center
2019

Institut Universitaire de Cardiologie et de Pneumologie de Québec
2018

Pulmonary arterial hypertension (PAH) is a vascular remodeling disease with poor prognosis and limited therapeutic options. Although the mechanisms contributing to in PAH are still unclear, several features, including hyperproliferation resistance apoptosis of pulmonary artery smooth muscle cells (PASMCs), have led emergence cancer-like concept. The molecular chaperone HSP90 (heat shock protein 90) directly associated malignant growth proliferation under stress conditions. In addition being...

10.1164/rccm.201708-1751oc article EN American Journal of Respiratory and Critical Care Medicine 2018-02-02

BReast Cancer Associated proteins 1 and 2 (BRCA1, −2) Partner Localizer of BRCA2 (PALB2) protein are tumour suppressors linked to a spectrum malignancies, including breast cancer Fanconi anemia. PALB2 coordinates functions BRCA1 during homology-directed repair (HDR) interacts with several chromatin proteins. In addition scaffold function, binds DNA. The functional role this interaction is poorly understood. We identified major DNA-binding site PALB2, mutations in which reduce RAD51 foci...

10.7554/elife.44063 article EN cc-by eLife 2019-04-24

Homologous recombination (HR) is a DNA repair mechanism of double-strand breaks and blocked replication forks, involving process homology search leading to the formation synaptic intermediates that are regulated ensure genome integrity. RAD51 recombinase plays central role in this mechanism, supported by its RAD52 BRCA2 partners. If mediator function load on RPA-ssDNA well established, HR still far from understood. We used transmission electron microscopy combined with biochemistry...

10.26508/lsa.202201751 article EN cc-by Life Science Alliance 2023-12-11

Abstract Replication-associated single-ended DNA double-strand breaks (seDSBs) are repaired predominantly through RAD51-mediated homologous recombination (HR). Removal of the non-homologous end-joining (NHEJ) factor Ku from resected seDSB ends is crucial for HR. The coordinated actions MRE11-CtIP nuclease activities orchestrated by ATM define one pathway eviction. Here, we identify pre-mRNA splicing protein XAB2 as a required resistance to seDSBs induced chemotherapeutic alkylator...

10.1093/nar/gkab785 article EN cc-by Nucleic Acids Research 2021-09-08

RAD51 is the central protein in DNA repair by homologous recombination (HR), involved several steps of this process. It shown that overexpression correlated with increased survival cancer cells to treatments. For past decade, overexpression-mediated resistance has justified development targeted inhibitors. One first molecules described inhibit was 4,4′-diisothiocyanato-stilbene-2,2′-disulfonic acid (DIDS) molecule. This small molecule effective inhibiting different functions RAD51, however...

10.3390/molecules26185460 article EN cc-by Molecules 2021-09-08

Abstract Homologous recombination (HR) is the most faithful DNA double-strand breaks (DSBs) repairing pathway. HR deficiency (HRD) can result from mutations in BRCA1, BRCA2, and PALB2, which are associated with genomic instability cancer. deficient cells survive through use of alternative repair pathways. Therefore, inhibiting these pathways HRD trigger cancer cell death. This phenomenon called synthetic lethality. The best-known example lethality that involving BRCA1/BRCA2/PALB2 PARP-1...

10.1158/1538-8514.synthleth24-a019 article EN Molecular Cancer Therapeutics 2024-06-10

Breast cancer associated proteins 1 and 2 (BRCA1, -2) partner localizer of BRCA2 (PALB2) protein are tumor suppressors linked to a spectrum malignancies, including breast Fanconi anemia. They stimulate RAD51 recombinase during homology-directed repair (HDR). Along with being hub for interaction network, PALB2 interacts DNA. The mechanism DNA binding its function poorly understood. We identified major DNA-binding site in PALB2, mutation which reduces the foci formation overall HDR efficiency...

10.1101/495192 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2018-12-13
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