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Cell, ISSN 0092-8674, 05/2018, Volume 173, Issue 4, pp. 972 - 988.e23
Repair of damaged DNA is essential for maintaining genome integrity and for preventing genome-instability-associated diseases, such as cancer. By combining... 
DNA damage repair | proximity labeling | shieldin | proteomics | 53BP1 | PARP inhibitors | telomere maintenance | antibody class-switch recombination | NHEJ | BRCA1 | PATHWAYS | CELLS | RESECTION | DAMAGE-RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CLASS-SWITCH RECOMBINATION | HOMOLOGOUS RECOMBINATION | DOUBLE-STRAND BREAK | TELOMERES | CELL BIOLOGY | Mad2 Proteins - metabolism | Humans | Ubiquitin-Protein Ligases - antagonists & inhibitors | DNA Breaks, Double-Stranded | Mad2 Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Telomere-Binding Proteins - genetics | RNA Interference | BRCA1 Protein - metabolism | Trans-Activators - genetics | Immunoglobulin Class Switching - drug effects | Nuclear Proteins - genetics | Telomere-Binding Proteins - metabolism | Tumor Suppressor p53-Binding Protein 1 - metabolism | DNA End-Joining Repair - drug effects | DNA-Binding Proteins - antagonists & inhibitors | Mutagenesis, Site-Directed | Tumor Suppressor p53-Binding Protein 1 - genetics | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Telomere-Binding Proteins - antagonists & inhibitors | Tumor Suppressor p53-Binding Protein 1 - antagonists & inhibitors | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | BRCA1 Protein - antagonists & inhibitors | Mad2 Proteins - genetics | Cell Line, Tumor | Trans-Activators - metabolism | Ubiquitin-Protein Ligases - genetics | RNA, Small Interfering - metabolism | DNA damage | Genomics | Antibodies | Genomes | DNA repair | Proteins | Viral antibodies | Telomeres | Evolutionary biology | Analysis | DNA | Genetic research | Mass spectrometry
Journal Article
Nature, ISSN 0028-0836, 2013, Volume 499, Issue 7456, pp. 50 - 54
53BP1 (also called TP53BP1) is a chromatin-associated factor that promotes immunoglobulin class switching and DNA double-strand-break (DSB) repair by... 
CRB2 | RECRUITMENT | FISSION YEAST | METHYLATION | CHROMATIN | DEPENDENT RESPONSE | RESECTION | MULTIDISCIPLINARY SCIENCES | SITES | DOUBLE-STRAND BREAKS | CLASS-SWITCH RECOMBINATION | Schizosaccharomyces pombe Proteins - chemistry | Histones - chemistry | Nucleosomes - chemistry | Humans | Ubiquitin - metabolism | Molecular Sequence Data | Male | Intracellular Signaling Peptides and Proteins - metabolism | DNA Breaks, Double-Stranded | DNA-Binding Proteins - deficiency | Cell Cycle Proteins - chemistry | Intracellular Signaling Peptides and Proteins - deficiency | Ubiquitination | Schizosaccharomyces pombe Proteins - metabolism | Female | Lysine - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Schizosaccharomyces | Protein Structure, Tertiary | Amino Acid Sequence | Cell Line | Signal Transduction | Cell Cycle Proteins - metabolism | Nucleosomes - metabolism | Mutant Proteins - metabolism | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Chromosomal Proteins, Non-Histone - deficiency | Amino Acid Motifs | Chromosomal Proteins, Non-Histone - genetics | Animals | Intracellular Signaling Peptides and Proteins - chemistry | Mutant Proteins - chemistry | Protein Binding | Mice | DNA Damage | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Chromosomal Proteins, Non-Histone - chemistry | Ubiquitin | Research | Properties | DNA repair | DNA damage | Proteins | DNA methylation | Mutation | Experiments | Recruitment
Journal Article
The American Journal of Human Genetics, ISSN 0002-9297, 11/2016, Volume 99, Issue 5, pp. 1190 - 1198
Uveal melanoma (UM) is a rare intraocular tumor that, similar to cutaneous melanoma, originates from melanocytes. To gain insights into its genetics, we... 
OCULAR MELANOMA | CELLS | COLORECTAL-CANCER | PROTEINS DLK1 | METASTASES | GENETICS & HEREDITY | RISK | EXPRESSION | RADIATION | SF3B1 | SOMATIC MUTATIONS | Melanoma - diagnosis | Exons | Humans | Middle Aged | Male | Phosphoproteins - metabolism | Case-Control Studies | RNA Splicing Factors - metabolism | DNA Copy Number Variations | Melanoma - genetics | Melanocytes - pathology | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Ubiquitin Thiolesterase - metabolism | Adult | Female | Membrane Proteins - metabolism | Eukaryotic Initiation Factor-1 - metabolism | GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism | Tumor Suppressor p53-Binding Protein 1 - metabolism | GTP-Binding Protein alpha Subunits, Gq-G11 - genetics | Uveal Neoplasms - genetics | Genome-Wide Association Study | Tumor Suppressor Proteins - metabolism | GTP-Binding Protein alpha Subunits - metabolism | Tumor Suppressor p53-Binding Protein 1 - genetics | Membrane Proteins - genetics | Eukaryotic Initiation Factor-1 - genetics | Ubiquitin-Protein Ligases - metabolism | GTP-Binding Protein alpha Subunits - genetics | Phosphoproteins - genetics | RNA Splicing Factors - genetics | Ubiquitin Thiolesterase - genetics | Skin Neoplasms | Uveal Neoplasms - diagnosis | Aged | Mutation | Ubiquitin-Protein Ligases - genetics | Genetic aspects | Nucleotide sequencing | Methods | Melanoma | DNA sequencing | Report
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 129, Issue 7, pp. 1415 - 1426
Protein kinases control cellular decision processes by phosphorylating specific substrates. Thousands of in vivo phosphorylation sites have been identified,... 
CELLBIO | ACTIVATION | DNA-DAMAGE RESPONSE | 53BP1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | SPECTROMETRY-BASED PROTEOMICS | ATM | EUKARYOTIC PROTEINS | PROTEIN-PHOSPHORYLATION | MASS-SPECTROMETRY | SIGNALING NETWORKS | CELL BIOLOGY | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Humans | DNA Repair Enzymes - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Phosphoproteins - metabolism | CDC2 Protein Kinase - metabolism | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | DNA Repair Enzymes - metabolism | Cell Cycle Proteins - genetics | DNA Damage - genetics | Proteomics - methods | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | CDC2 Protein Kinase - genetics | Computational Biology - methods | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Repressor Proteins - genetics | Ataxia Telangiectasia Mutated Proteins | Binding Sites - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Glycogen Synthase Kinase 3 - genetics | Signal Transduction - physiology | Software | Tumor Suppressor p53-Binding Protein 1
Journal Article
Nature, ISSN 0028-0836, 02/2013, Volume 494, Issue 7438, pp. 502 - 505
Mammalian telomeres repress DNA-damage activation at natural chromosome ends by recruiting specific inhibitors of the DNA-damage machinery that form a... 
UBIQUITINATION | RECOMBINATION | MAINTENANCE | COMPLEX | REPAIR | MAMMALIAN TELOMERES | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | CELL-CYCLE | PROTEINS | TRF2 | Tumor Suppressor Proteins - antagonists & inhibitors | Chromosomes, Mammalian - genetics | Protein Multimerization | Ubiquitin-Protein Ligases - antagonists & inhibitors | Telomeric Repeat Binding Protein 2 - chemistry | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Telomere - metabolism | Protein-Serine-Threonine Kinases - metabolism | Telomere - genetics | Protein Structure, Tertiary | Endopeptidases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - metabolism | Signal Transduction | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Ataxia Telangiectasia Mutated Proteins | Endopeptidases - deficiency | Protein Transport | Animals | DNA Repair | Telomeric Repeat Binding Protein 2 - metabolism | Mice | DNA Damage | Enzyme Activation | Tumor Suppressor p53-Binding Protein 1 | Chromosomes, Mammalian - metabolism | Telomeres | Research | Binding proteins | Observations | Properties | DNA damage | Proteins | Enzymes | DNA methylation | Amino acids | Agreements | Telomerase | Chromosomes | RNF168 | Brca1 | genomic stability | telomere | ATM | NHEJ
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 7/2010, Volume 190, Issue 2, pp. 197 - 207
The signaling cascade initiated in response to DNA double-strand breaks (DSBs) has been extensively investigated in interphase cells. Here, we show that... 
Phosphorylation | Chromatin | Mitosis | DNA damage | Ubiquitins | Cell cycle | Cell lines | Histones | Antibodies | Reports | Chromosomes | REPAIR PROTEINS | RECRUITMENT | PHOSPHORYLATION | HUMAN-CELLS | 53BP1 | HISTONE H2AX | ATM | CHECKPOINT | IONIZING-RADIATION | RNF8 UBIQUITIN LIGASE | CELL BIOLOGY | Humans | Intracellular Signaling Peptides and Proteins - metabolism | DNA Breaks, Double-Stranded | Recombinant Fusion Proteins - metabolism | DNA-Binding Proteins - metabolism | DNA-Activated Protein Kinase - genetics | DNA-Activated Protein Kinase - metabolism | Tumor Suppressor Proteins - genetics | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Cell Line | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Histones - genetics | Mitosis - physiology | DNA Repair | Recombinant Fusion Proteins - genetics | Signal Transduction - physiology | Trans-Activators - metabolism | DNA Damage | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Ubiquitin-Protein Ligases - genetics | DNA | Research
Journal Article
Science, ISSN 0036-8075, 5/2012, Volume 336, Issue 6081, pp. 593 - 597
The telomere end-protection problem is defined by the aggregate of DNA damage signaling and repair pathways that require repression at telomeres. To define the... 
Telomeres | Yeasts | Quantification | Lymphocytes | DNA | DNA damage | REPORTS | Cell cycle | Ataxia telangiectasia | Repression | Chromosomes | JOINING PATHWAY | POT1 PROTEINS | MAMMALIAN TELOMERES | SGS1 | MULTIDISCIPLINARY SCIENCES | DYSFUNCTIONAL TELOMERES | DOUBLE-STRAND BREAKS | HOMOLOGOUS RECOMBINATION | NHEJ | YEAST KU | Telomere - ultrastructure | Antigens, Nuclear - metabolism | Telomeric Repeat Binding Protein 1 - genetics | Telomeric Repeat Binding Protein 1 - metabolism | Homologous Recombination | DNA Breaks, Double-Stranded | DNA Ligases - metabolism | DNA-Binding Proteins - metabolism | Poly-ADP-Ribose Binding Proteins | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | Telomere - metabolism | Telomere-Binding Proteins - metabolism | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | Chromosomal Proteins, Non-Histone - metabolism | Signal Transduction | Cell Cycle Proteins - metabolism | Cells, Cultured | Ataxia Telangiectasia Mutated Proteins | Xenopus Proteins | DNA-Binding Proteins - genetics | Telomere Homeostasis | Mice, Knockout | Poly(ADP-ribose) Polymerases - metabolism | Animals | Antigens, Nuclear - genetics | Cell Cycle | Ku Autoantigen | DNA Repair | DNA Ligase ATP | Telomeric Repeat Binding Protein 2 - metabolism | Mice | Poly (ADP-Ribose) Polymerase-1 | Telomeric Repeat Binding Protein 2 - genetics | Tumor Suppressor p53-Binding Protein 1 | Proteins | Physiological aspects | Research | Health aspects | DNA repair | Telomerase
Journal Article
Molecular Cell, ISSN 1097-2765, 10/2016, Volume 64, Issue 1, pp. 51 - 64
The tumor suppressor protein 53BP1, a pivotal regulator of DNA double-strand break (DSB) repair, was first identified as a p53-interacting protein over two... 
BRCT DOMAINS | ACTIVATION | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | V(D)J RECOMBINATION | TUMOR-SUPPRESSOR | CLASS-SWITCH RECOMBINATION | P53 PATHWAY | PROTEINS | CELL BIOLOGY | Gamma Rays | Endonucleases - genetics | Tumor Suppressor p53-Binding Protein 1 - chemistry | RNA, Guide - genetics | RNA, Guide - metabolism | Humans | Protein Multimerization | CRISPR-Associated Protein 9 | Endonucleases - metabolism | DNA Breaks, Double-Stranded | Tumor Suppressor Protein p53 - genetics | MCF-7 Cells | Base Sequence | Clustered Regularly Interspaced Short Palindromic Repeats | Ubiquitin Thiolesterase - metabolism | Protein Interaction Domains and Motifs | Binding Sites | Tumor Suppressor p53-Binding Protein 1 - metabolism | Promoter Regions, Genetic | Protein Conformation, alpha-Helical | Tumor Suppressor p53-Binding Protein 1 - genetics | Signal Transduction | Bacterial Proteins - genetics | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Ubiquitin Thiolesterase - genetics | Gene Editing | Protein Conformation, beta-Strand | DNA Repair | Protein Binding | Bacterial Proteins - metabolism | Tumor Suppressor Protein p53 - chemistry | Ubiquitin Thiolesterase - chemistry | Oligomers | Ubiquitin | Ionizing radiation | Chromatin | Proteases | Genes | Genomics | DNA | Tumor proteins | DNA repair
Journal Article
Nature, ISSN 0028-0836, 2015, Volume 521, Issue 7553, pp. 541 - U308
Journal Article
Molecular Cell, ISSN 1097-2765, 02/2017, Volume 65, Issue 4, pp. 671 - 684.e5
Canonical non-homologous end joining (c-NHEJ) repairs DNA double-strand breaks (DSBs) in G1 cells with biphasic kinetics. We show that DSBs repaired with slow... 
non-homologous end joining | DNA double-strand breaks | resection | nucleases | FACILITATES REPAIR | DAMAGE RESPONSE | TUMOR SUPPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | NUCLEASE ACTIVITIES | CTIP | DEPENDENT PROTEIN-KINASE | REPAIR PATHWAY CHOICE | CELL-CYCLE | BRCA1 | BINDING | CELL BIOLOGY | Translocation, Genetic | Phosphorylation | DNA End-Joining Repair - radiation effects | Humans | DNA Repair Enzymes - genetics | DNA Breaks, Double-Stranded | Cell Nucleus - enzymology | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Transfection | Time Factors | Cell Nucleus - pathology | Cell Nucleus - radiation effects | BRCA1 Protein - metabolism | Gene Deletion | DNA Repair Enzymes - metabolism | G2 Phase | Exodeoxyribonucleases - genetics | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor p53-Binding Protein 1 - metabolism | Tumor Suppressor p53-Binding Protein 1 - genetics | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | BRCA1 Protein - genetics | Carrier Proteins - genetics | Carrier Proteins - metabolism | G1 Phase - radiation effects | Endonucleases | Exodeoxyribonucleases - metabolism | HeLa Cells | Kinetics | Biotechnology | Nucleases | Surgery | Genomics | DNA | DNA binding proteins | DNA repair
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/2011, Volume 108, Issue 36, pp. 14944 - 14949
The bacterial pathogen Helicobacter pylori chronically infects the human gastric mucosa and is the leading risk factor for the development of gastric cancer.... 
Helicobacter pylori | Epithelial cells | DNA damage | DNA | Cell nucleus | Cell lines | Bacteria | Cultured cells | Infections | Mice | Chromosome breaks | DNA damage signaling | Gastric tumorigenesis | Genomic instability | CYTOLETHAL DISTENDING TOXIN | MULTIDISCIPLINARY SCIENCES | RISK | MISMATCH REPAIR | COLONIZATION | GENETIC INSTABILITY | EPITHELIAL-CELLS | chromosome breaks | GASTRIC-CANCER | INFLAMMATION | INFECTION | MICE | genomic instability | gastric tumorigenesis | Phosphorylation | Epithelial Cells - metabolism | Humans | Stomach Neoplasms - metabolism | Helicobacter Infections - complications | Stomach Neoplasms - pathology | Intracellular Signaling Peptides and Proteins - metabolism | Antigens, Bacterial - genetics | DNA Breaks, Double-Stranded | Helicobacter Infections - pathology | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Helicobacter Infections - metabolism | Nuclear Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Stomach Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Chromosomal Proteins, Non-Histone - metabolism | Bacterial Proteins - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Genomic Islands | Epithelial Cells - pathology | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Chromosomal Proteins, Non-Histone - genetics | Bacterial Adhesion | Stomach Neoplasms - microbiology | Animals | Histones - genetics | Helicobacter pylori - metabolism | Epithelial Cells - microbiology | Chromosome Aberrations | Cell Line, Tumor | Bacterial Proteins - metabolism |