A5017007013- Epigenetics and DNA Methylation
- DNA Repair Mechanisms
- Genomics and Chromatin Dynamics
- Extracellular vesicles in disease
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Chronic Myeloid Leukemia Treatments
- RNA modifications and cancer
- Chronic Lymphocytic Leukemia Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer-related molecular mechanisms research
- Multiple Myeloma Research and Treatments
- Ubiquitin and proteasome pathways
- Immune cells in cancer
- Protein Degradation and Inhibitors
- Immune Response and Inflammation
- Systemic Sclerosis and Related Diseases
- MicroRNA in disease regulation
- Mesenchymal stem cell research
- Fibroblast Growth Factor Research
- Genetics and Neurodevelopmental Disorders
- Cytokine Signaling Pathways and Interactions
- Kruppel-like factors research
- Pharmacological Effects and Toxicity Studies
- Protein Kinase Regulation and GTPase Signaling
- 14-3-3 protein interactions
Centro di Riferimento Oncologico della Basilicata
2012-2016
Institute for Experimental Endocrinology and Oncology
2007-2016
Istituti di Ricovero e Cura a Carattere Scientifico
2012-2015
University of Naples Federico II
2004-2012
University of Central Florida
2011
Universitat de Barcelona
2004
To explore the link between DNA damage and gene silencing, we induced a double-strand break in genome of Hela or mouse embryonic stem (ES) cells using I-SceI restriction endonuclease. The site lies within one copy two inactivated tandem repeated green fluorescent protein (GFP) genes (DR-GFP). A total 2%–4% generated functional GFP by homology-directed repair (HR) conversion. However, ~50% these recombinants expressed poorly. Silencing was rapid associated with HR methylation recombinant...
// Luciana De Luca 1 , Stefania Trino Ilaria Laurenzana Vittorio Simeon Giovanni Calice Raimondo 2 Marina Podestà 3 Michele Santodirocco 4 Lazzaro Di Mauro Francesco La Rocca Antonella Caivano Annalisa Morano Frassoni 5 Daniela Cilloni Luigi Del Vecchio 6, 7, * Pellegrino Musto 8, Laboratory of Preclinical and Translational Research, IRCCS-Centro di Riferimento Oncologico della Basilicata (CROB), Rionero in Vulture, 85028, Italy Department Clinical Biological Sciences, University...
Abstract We characterize the changes in chromatin structure, DNA methylation and transcription during after homologous repair (HR). find that HR modifies pattern of repaired segment. also alters local histone H3 as well structure by inducing DNA-chromatin loops connecting 5′ 3′ ends gene. During a two-week period repair, transcription-associated demethylation promoted Base Excision Repair enzymes further DNA. Subsequently, genes display stable but diverse profiles. These profiles govern...
Reactive oxygen species (ROS) are signaling molecules that mediate stress response, apoptosis, DNA damage, gene expression and differentiation. We report here differentiation of oligodendrocytes (OLs), the myelin forming cells in CNS, is driven by ROS. To dissect OL pathway, we used cell line MO3-13, which display molecular cellular features precursors. These exposed 1-4 days to low levels H2O2 or protein kinase C (PKC) activator, phorbol-12-Myristate-13-Acetate (PMA) increased specific...
In this work, we examine regulation of DNA methyltransferase 1 (DNMT1) by the damage inducible protein, GADD45α. We used a system to induce homologous recombination (HR) at unique double-strand break in GFP reporter mammalian cells. After HR, repaired is hypermethylated recombinant clones showing low expression (HR-L expressor class), while high recombinants (HR-H clones) previous methylation patterns are erased. GADD45α, which transiently induced breaks, binds chromatin undergoing HR...
Dual Oxidases (DUOX) 1 and 2 are efficiently expressed in thyroid, gut, lung immune system. The function the regulation of these enzymes mammals still largely unknown. We report here that DUOX human neuroblastoma SK-N-BE cells as well a oligodendrocyte cell line (MO3-13) rat brain they induced by platelet derived growth factor (PDGF). levels proteins mRNAs reactive oxygen species (ROS) produced membrane NADPH oxidase. As to mechanism, we find PDGF stimulates oxidase produce ROS, which...
MAPK phosphorylation of various substrates is mediated by the presence docking sites, including D domain and DEF motif. Depending on number sequences these domains, are phosphorylated specific subsets MAPKs. For example, a targets JNK to c-Jun, whereas motif required for ERK c-Fos. JunD, in contrast, contains both domains. Here we show that motifs mediate JunD response either or activation. An intact activation subtypes MAPK. The acts together with elicit efficient epidermal growth factor...
// Roberto Ria 1, * , Vittorio Simeon 2, Assunta Melaccio 1 Giovanna Di Meo 3 Stefania Trino 2 Carmela Mazzoccoli Ilaria Saltarella Aurelia Lamanuzzi Annalisa Morano Angela Gurrado Alessandro Pasculli Gaetano Lastilla 4 Pellegrino Musto Antonia Reale Franco Dammacco Angelo Vacca Mario Testini Department of Biomedical Sciences and Human Oncology, Section Internal Medicine "G. Baccelli", Bari, BA, Italy Laboratory Pre-Clinical Traslational Research, IRCSS CROB, Rionero in Vulture, PZ, Unit...
Objectives: Here we evaluated the neuroprotective effects of two well‐known mood stabilizers, lithium and valproic acid (VPA), against colchicine neurotoxicity in cerebellar granule cells (CGNs). Methods: The CGNs were differentiated for 7 days, pretreated with or VPA 24 h after 1 μ M was added. Cellular damage assessed 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium (MTT) method apoptosis characterized by chromatin condensation DNA fragmentation. Results: Incubation (1–5 mM)...
Endocytosis is the major regulator process of tyrosine kinase receptor (RTK) functional activities. Bridging integrator 1 (BIN1) a key protein involved in RTK intracellular trafficking. Here, we report, by studying 34 patients with chronic myeloid leukemia (CML) at diagnosis, that BIN1 gene downregulated CML as compared to healthy controls, suggesting an altered endocytosis RTKs. Rab interactor (RIN1), activator BIN1, displayed similar behavior. Treatment 57 inhibitors caused, along BCR-ABL1...
This work is aimed at the dissection of molecular mechanism(s) linking DNA damage and gene silencing. To this end, we have developed a genetic system that allows rapid assessment homologous-directed repair (HR) an unique DNA double strand break (DSB). Briefly, induced DBS in genome HeLa or mouse embryonic stem (ES) cells using I-SceI restriction endonuclease. Homologous recombination by conversion, initiated site the double break, converts 2 inactivated tandem repeated green...