A5102026942- DNA Repair Mechanisms
- Carcinogens and Genotoxicity Assessment
- Mitochondrial Function and Pathology
- DNA and Nucleic Acid Chemistry
- Genetic factors in colorectal cancer
- Cytomegalovirus and herpesvirus research
- Cancer-related Molecular Pathways
- Telomeres, Telomerase, and Senescence
- Genomics and Chromatin Dynamics
- Coenzyme Q10 studies and effects
- CRISPR and Genetic Engineering
- Metabolism and Genetic Disorders
- HIV Research and Treatment
- Acute Lymphoblastic Leukemia research
- RNA modifications and cancer
- Cancer Genomics and Diagnostics
- Adipose Tissue and Metabolism
- Herpesvirus Infections and Treatments
- Immune Cell Function and Interaction
- Advanced biosensing and bioanalysis techniques
- Adipokines, Inflammation, and Metabolic Diseases
- HIV/AIDS drug development and treatment
- Cancer, Hypoxia, and Metabolism
- RNA and protein synthesis mechanisms
- RNA Research and Splicing
Istituto Superiore di Sanità
2006-2021
Istituto di Genetica Molecolare
2007
National Research Council
2007
National Institute of Environmental Health Sciences
1998
The base excision repair (BER) of modified nucleotides is initiated by damage-specific DNA glycosylases. the resulting apurinic/apyrimidinic site involves replacement either a single nucleotide (short patch BER) or several (long BER). mechanism that controls selection BER pathway unknown. We tested hypothesis type damage present on DNA, determining specific glycosylase in charge its excision, drives abasic intermediate to branch. In mammalian cells hypoxanthine (HX) and 1,N 6-ethenoadenine...
Mammalian cells possess two distinct pathways for completion of base excision repair (BER): the DNA polymerase β (Pol β)-dependent short-patch pathway (replacement one nucleotide), which is main route, and long-patch (resynthesis 2−6 nucleotides), PCNA-dependent. To address issue how these share their role in BER ability Pol β-defective mammalian cell extracts to a single abasic site constructed circular duplex plasmid molecule was tested standard vitro reaction. β-deficient were able...
Abstract The OGG1 and MYH DNA glycosylases prevent the accumulation of 8-hydroxyguanine. In Myh−/− mice, there was no time-dependent 8-hydroxyguanine in brain, small intestine, lung, spleen, or kidney. Liver an exception to this general pattern. Inactivation both caused age-associated lung intestine. effects abrogated on hepatic levels were additive. Because is increased incidence intestine cancer Myh−/−/Ogg1−/− these findings support a causal role for unrepaired oxidized bases development.
It has been hypothesized that a replication associated repair pathway operates on base damage and single strand breaks (SSB) at forks. In this study, we present the isolation from nuclei of human cycling cells multiprotein complex containing most essential components excision (BER)/SSBR, including APE1, UNG2, XRCC1 POLβ, DNA PK, replicative POLα, δ ɛ, ligase 1 cell cycle regulatory protein cyclin A. Co-immunoprecipitation revealed in proteins are physically to A MCM7. This is endowed with...
CS proteins have been involved in the repair of a wide variety DNA lesions. Here, we analyse role break by studying histone H2AX phosphorylation different cell cycle phases and comet assay CS-A CS-B primary transformed cells. Following methyl methane sulphate treatment significant accumulation unrepaired single strand breaks was detected cells as compared to normal cells, leading double S G2 phases. A delay DSBs were also observed following IR exposure. These data confirm CSB suppression...
Cockayne Syndrome (CS) is an autosomal recessive neurodegenerative premature aging disorder associated with defects in nucleotide excision repair (NER). Cells from CS patients, mutations CSA or CSB genes, present elevated levels of reactive oxygen species (ROS) and are defective the a variety oxidatively generated DNA lesions. In this study, six purine lesions were ascertained wild type (wt) CSA, wtCSB CSB-transformed fibroblasts under different tensions (hyperoxic 21%, physioxic 5% hypoxic...
DNA repair gene expression in a set of gastric cancers suggested an inverse association between the mismatch (MMR) MLH1 and that base excision (BER) polymerase β (Polβ). To gain insight into possible crosstalk these two pathways cancer, we analysed human adenocarcinoma AGS cells over-expressing Polβ or active site mutants, alone combination with silencing. Next, investigated cellular response to alkylating agent methyl methanesulfonate (MMS) purine analogue 6-thioguanine (6-TG), agents...
Xeroderma Pigmentosum (XP) is a DNA repair disease characterized by nucleotide excision (NER) malfunction, leading to photosensitivity and increased incidence of skin malignancies. The role XP-A in NER pathways has been well studied while discrepancies associated with ROS levels the radical species between normal deficient XPA cell lines have observed. Using liquid chromatography tandem mass spectrometry we determined four 5’,8-cyclopurines (cPu) lesions (i.e., 5′R-cdG, 5′S-cdG, 5′R-cdA...
In this article, we report the establishment of persistent HIV type 1 infection normal Swiss mice after a single intraperitoneal injection with high-producing HIV-infected U937 cells. Anti-HIV antibodies were found more than 500 days original injection, and p24 antigenemia was detected in approximately 50% mice. By polymerase chain reaction (PCR) techniques, HIV-specific gag env sequences DNA samples from peripheral blood mononuclear cells (PBMC) peritoneal seropositive 300 to inoculation...