Articles+Catalog Search Results

MAD2L2 regulates DNA repair at deprotected telomeres and at ionizing-radiation-induced double-stranded DNA breaks by inhibiting resection of the 5′ ends... 13/106, 13/109, 13/31, 13/44, 13/51, 13/89, 14/19, 14/32, 38/1, 38/70, 42/35, 45/77, 45/90, 631/337/103/560, 631/337/1427, 631/67/68, 631/80/103/560, 82/29, 82/80, Analysis, Ataxia Telangiectasia Mutated Proteins - metabolism, Carrier Proteins - metabolism, Cell Line, Tumor, Deoxyribonucleic acid, DNA, DNA binding proteins, DNA Breaks, Double-Stranded - radiation effects, DNA damage, DNA End-Joining Repair - genetics, DNA polymerases, DNA repair, DNA Repair Enzymes - metabolism, DNA Replication, DNA-Binding Proteins - metabolism, Exodeoxyribonucleases - metabolism, Genetic research, Genetic screening, Genomic Instability, Genomics, Humanities and Social Sciences, Humans, Intracellular Signaling Peptides and Proteins - metabolism, Irradiation, Kinases, letter, Mad2 Proteins - metabolism, multidisciplinary, Nuclear Proteins - metabolism, Phosphorylation, Recombinational DNA Repair - genetics, Repressor Proteins, Science, Telomerase, Telomere - genetics, Telomere - metabolism, Telomere-Binding Proteins - metabolism, Telomeres, Tumor Suppressor p53-Binding Protein 1, Ubiquitin-Protein Ligases - metabolism

.... A-T is causally linked to defects in ATM, a master regulator of the response to and repair of DNA double-strand breaks... Animals, Ataxia Telangiectasia - pathology, Ataxia Telangiectasia Mutated Proteins - deficiency, Ataxia Telangiectasia Mutated Proteins - metabolism, Behavior, Animal, Caenorhabditis elegans - metabolism, Caenorhabditis elegans - ultrastructure, Cells, Cultured, Disease Models, Animal, DNA Repair - drug effects, Gene Knockdown Techniques, Health, Homeostasis - drug effects, Longevity - drug effects, Metabolomics, Mice, Mitophagy - drug effects, NAD - pharmacology, Neurons - drug effects, Neurons - metabolism, Phenotype, Phthalazines - pharmacology, Piperazines - pharmacology, Proteomics, Rats, Sprague-Dawley, Signal Transduction - drug effects, Sirtuin 1 - metabolism

Emerging findings suggest that compromised cellular bioenergetics and DNA repair contribute to the pathogenesis of Alzheimer’s disease (AD... Aging, Alzheimer Disease, Alzheimer's disease, Animals, Apoptosis, Behavioral plasticity, Bioenergetics, Biological Sciences, Brain, Cognitive ability, Cognitive Dysfunction, Damage accumulation, Degeneration, Deoxyribonucleic acid, Disease Models, Animal, DNA, DNA Damage, DNA repair, Energy metabolism, Gene Expression Regulation - drug effects, Genotypes, Hippocampal plasticity, Hippocampus, Inflammation, Male, Metabolism, Mice, Mice, Transgenic, NAD, NAD - pharmacology, NAD supplementation, NADH, Neurodegeneration, Neurodegenerative diseases, Neurogenesis - drug effects, Neurons, Niacinamide - analogs & derivatives, Niacinamide - pharmacology, Nicotinamide, Nicotinamide adenine dinucleotide, Nicotinamide riboside, Pathogenesis, Pathology, Phosphorylation, PNAS Plus, Pyridinium Compounds, Repair, Rodents, Sirtuin 3 - genetics, Sirtuin 3 - metabolism, Sirtuins - genetics, Sirtuins - metabolism, Supplements, Synaptic plasticity, Tau protein, tau Proteins - metabolism, β-Amyloid

Uracil‐DNA glycosylases (UDGs) are evolutionarily conserved DNA repair enzymes that initiate the base excision repair pathway and remove uracil from DNA... Bacteriology, Base excision repair, Catalysis, Deoxyribonucleic acid, DNA, DNA - drug effects, DNA - metabolism, DNA glycosylase, DNA mimicry, DNA Repair, Enzymes, Humans, Mimicry, Molecular Mimicry, Protein Conformation, Repair, Reviews, Structure-function relationships, Substrate Specificity, Substrates, Uracil, Uracil-DNA Glycosidase - antagonists & inhibitors, Uracil-DNA Glycosidase - chemistry, Uracil-DNA Glycosidase - metabolism, uracil-DNA glycosylase

Germline aberrations in critical DNA-repair and DNA damage-response (DDR) genes cause cancer predisposition, whereas various tumors harbor somatic mutations causing defective DDR/DNA repair... Animals, Antineoplastic Agents - pharmacology, Antineoplastic Agents - therapeutic use, DNA Repair - drug effects, Drug Screening Assays, Antitumor, Genetic Predisposition to Disease, Humans, Mutation, Neoplasms - drug therapy, Neoplasms - genetics, Poly(ADP-ribose) Polymerase Inhibitors - pharmacology, Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use

... ( SDHA , SDHB , SDHC and SDHD ), respectively 2 – 4 . Recent work has made an unexpected connection between these metabolites and DNA repair by showing that they suppress the pathway of homology-dependent repair (HDR... 14, 14/63, 38, 631/67/1922, 631/67/2327, 631/67/68/2486, Adenosine diphosphate, Ataxia Telangiectasia Mutated Proteins - metabolism, Cell cycle, Cell Line, Tumor, Chromatin, Chromatin - drug effects, Chromatin - metabolism, Clinical trials, Control, Defects, Dehydrogenase, Dehydrogenases, Deoxyribonucleic acid, Deregulation, Disruption, DNA, DNA Breaks - drug effects, DNA damage, DNA repair, DNA Repair - drug effects, Fumarase, Gene expression, Genes, Genomes, Homologous Recombination - drug effects, Homology, Humanities and Social Sciences, Humans, Influence, Isocitrate dehydrogenase, Jumonji Domain-Containing Histone Demethylases - antagonists & inhibitors, Ligands, Lysine, Lysine Acetyltransferase 5 - metabolism, Masking, Metabolites, Methylation - drug effects, multidisciplinary, Mutation, Neoplasms - drug therapy, Neoplasms - genetics, Neoplasms - metabolism, Neoplasms - pathology, Phosphorylation, Poly(ADP-ribose) polymerase, Poly(ADP-ribose) Polymerase Inhibitors - pharmacology, Recruitment, Repair, Ribose, Science, Science (multidisciplinary), Signal transduction, Signal Transduction - drug effects, Succinate dehydrogenase, Tumors

DNA-protein crosslinks (DPCs) are highly toxic DNA lesions because they interfere with DNA transactions... Animals, DNA Damage - genetics, DNA repair, DNA Repair - genetics, DNA Repair Enzymes - genetics, DNA-Binding Proteins - genetics, DNA-Binding Proteins - metabolism, DNA-protein crosslinks, DPC protease, DVC1, Genomic Instability, Humans, Recombination, Genetic, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins - genetics, Saccharomyces cerevisiae Proteins - metabolism, Spartan, SPRTN, Wss1

The error-free and efficient repair of DNA double-stranded breaks (DSBs) is extremely important for cell survival... 14/19, 38/15, 38/23, 38/91, 631/337/1427, 631/337/384, A549 Cells, Cell Line, Tumor, Cell survival, Damage, DEAD-box RNA Helicases - genetics, DEAD-box RNA Helicases - metabolism, Deoxyribonucleic acid, DNA, DNA - genetics, DNA - metabolism, DNA Breaks, Double-Stranded, DNA Damage, DNA End-Joining Repair, DNA Repair, DNA sequencing, Gene Expression Profiling, Homologous Recombination, Homology, Humanities and Social Sciences, Humans, Hybrids, miRNA, multidisciplinary, Non-homologous end joining, Repair, Ribonuclease III - genetics, Ribonuclease III - metabolism, Ribonucleic acid, RNA, RNA - genetics, RNA - metabolism, RNA Interference, RNA processing, Science, Science (multidisciplinary)

The DNA damage response (DDR) generates transient repair compartments to concentrate repair proteins and activate signaling factors... 53BP1, Adaptor Proteins, Signal Transducing - metabolism, Animals, Assembly, Cell activation, Cell Cycle Proteins - metabolism, Cell fate, Cell Line, Tumor, Clustering, Compartments, CRISPR, CRISPR-Cas Systems, Damage accumulation, Damage detection, Damage localization, Deoxyribonucleic acid, Disruption, DNA, DNA damage, DNA damage response, DNA Repair, Dogs, Droplets, EMBO09, EMBO13, Gene expression, genome stability, Histones - metabolism, Humans, Hydrophobicity, Liquid-Liquid Extraction - methods, liquid–liquid phase separation, Madin Darby Canine Kidney Cells, MCF-7 Cells, Optogenetics, Osmosis, Osmotic Pressure, p53, p53 Protein, Phase separation, Physicochemical properties, Proteins, Repair, Stress, Physiological, Tumor suppressor genes, Tumor Suppressor p53-Binding Protein 1 - genetics, Tumor Suppressor p53-Binding Protein 1 - metabolism, Tumor Suppressor Protein p53 - metabolism, Tumors