A5068468331- DNA Repair Mechanisms
- Cancer-related Molecular Pathways
- Genomics and Chromatin Dynamics
- CRISPR and Genetic Engineering
- PARP inhibition in cancer therapy
- Cancer, Hypoxia, and Metabolism
- Nanoplatforms for cancer theranostics
- Cell death mechanisms and regulation
- Peptidase Inhibition and Analysis
- RNA modifications and cancer
- Immunodeficiency and Autoimmune Disorders
- Viral-associated cancers and disorders
- Cancer Research and Treatments
- RNA Research and Splicing
- Radiation Therapy and Dosimetry
- Advanced Radiotherapy Techniques
- BRCA gene mutations in cancer
- Genomics and Phylogenetic Studies
- Genetics and Neurodevelopmental Disorders
- Peroxisome Proliferator-Activated Receptors
- 14-3-3 protein interactions
- RNA Interference and Gene Delivery
- Glutathione Transferases and Polymorphisms
- Cancer Mechanisms and Therapy
- Drug Transport and Resistance Mechanisms
Harvard University
2014-2024
Dana-Farber Cancer Institute
2017-2024
Dana-Farber Brigham Cancer Center
2020-2024
Brigham and Women's Hospital
2020-2024
Inserm
1995-2010
Centre National de la Recherche Scientifique
2001-2010
Institut de génétique et de biologie moléculaire et cellulaire
2004-2010
Université de Strasbourg
2010
Institut de Radiobiologie Cellulaire et Moléculaire
2007
Commissariat à l'Énergie Atomique et aux Énergies Alternatives
2001-2006
The histone variant H3.3 marks active chromatin by replacing the conventional H3.1. In this study, we investigate detailed mechanism of replication-independent deposition. We found that death domain-associated protein DAXX and remodeling factor ATRX (α-thalassemia/mental retardation syndrome protein) are specifically associated with deposition machinery. Bacterially expressed has a marked binding preference for assists (H3.3–H4) 2 tetramers on naked DNA, thus showing is chaperone....
Mutations in the XPD subunit of TFIIH give rise to human genetic disorders initially defined as DNA repair syndromes. Nevertheless, xeroderma pigmentosum (XP) group D (XP-D) patients develop clinical features such hypoplasia adipose tissue, implying a putative transcriptional defect. Knowing that peroxisome proliferator-activated receptors (PPARs) are implicated lipid metabolism, we investigated expression PPAR target genes tissues and livers XPD-deficient mice found (i) some abnormally...
As nanoparticle solutions move towards human clinical trials in radiation therapy, the influence of key beam parameters on therapeutic efficacy must be considered. In this study, we have investigated therapy delivery variables that may significantly affect nanoparticle-mediated dose amplification. We found a benefit for situations which increased proportion low energy photons incident beam. Most notably, "unflattened" photon beams from linear accelerator results improved outcomes relative to...
Purpose: γ-irradiation leads to activation of p53 tumour suppressor gene and p53-dependant stimulation a large panel cellular genes including proapoptotic involved in intrinsic extrinsic pathways. Most vivo published data referred high (lethal) irradiation doses. The present study was performed analyse the p53-dependent response more relevant low
Recent data showed that p53 stimulates the expression of genes encoding not only pro- but also antioxidant enzymes. It was suggested could be induced under physiologic levels stress while prooxidant ones respond to higher level stress. Results presented in this article illustrate an additional degree complexity. We show Haeme-oxygenase 1 (HO-1), a stress-inducible gene codes for enzyme having properties, is stimulated p53-dependent manner thymus and spleen irradiated mice. prove HO-1 direct...
Abstract We previously demonstrated that human C3d or pep16, a 16‐amino acid synthetic peptide derived from C3d, induced in vivo and vitro tyrosine phosphorylation of pp105, an intracellular component found only cells express CR2 at their surface. To determine the contribution molecules to this enzymatic regulation, we first analyzed whether activation by other extracellular ligands could trigger such regulation cell extracts. Subsequently, used extracts either CR2‐positive depleted...
Abstract The recruitment of 53BP1 to chromatin, mediated by its recognition histone H4 dimethylated at lysine 20 (H4K20me2), is important for DNA double-strand break repair. Using a series small molecule antagonists, we demonstrate conformational equilibrium between an open and pre-existing lowly populated closed state in which the H4K20me2 binding surface buried interface two interacting molecules. In cells, these antagonists inhibit chromatin wild type 53BP1, but do not affect variants...
Abstract High-grade serous ovarian carcinoma (HGSOC) patients with germline mutations in BRCA1/2 exhibit high sensitivity and improved outcome to double strand DNA break (DSB)-inducing agents [i.e. platinum Poly(ADP-ribose) polymerase inhibitors (PARPi)] due underlying defects repair via homologous recombination (HR). Due their effectiveness, three PARP (olaparib, rucaparib, niraparib) have recently gained FDA approval for the treatment of HGSOCs. However, de novo acquired resistance these...