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Nature cell biology, ISSN 1476-4679, 2018, Volume 20, Issue 8, pp. 954 - 965
BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors... 
PATHWAY CHOICE | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | 53BP1 | CLASS-SWITCH RECOMBINATION | FANCONI-ANEMIA | DIFFERENTIAL EXPRESSION ANALYSIS | POLYMERASE-ZETA | TELOMERES | CELL BIOLOGY | Osteosarcoma - drug therapy | Mad2 Proteins - metabolism | Humans | Multiprotein Complexes | Ovarian Neoplasms - pathology | Bone Neoplasms - pathology | DNA Breaks, Double-Stranded | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Ovarian Neoplasms - genetics | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | HEK293 Cells | Female | Bone Neoplasms - genetics | Ovarian Neoplasms - metabolism | Bone Neoplasms - drug therapy | BRCA1 Protein - deficiency | Telomere-Binding Proteins - metabolism | Ovarian Neoplasms - drug therapy | Osteosarcoma - metabolism | DNA-Binding Proteins | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinational DNA Repair | Tumor Suppressor p53-Binding Protein 1 - genetics | Cisplatin - pharmacology | Breast Neoplasms - drug therapy | Proteins - genetics | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Breast Neoplasms - genetics | Proteins - metabolism | Breast Neoplasms - pathology | Mad2 Proteins - genetics | Cell Line, Tumor | Mice | Osteosarcoma - genetics | Cell Cycle Proteins | Osteosarcoma - pathology | Care and treatment | DNA | Cancer cells | Breast cancer | Genetic aspects | Research | Gene expression | Single-stranded DNA | DNA damage | Homologous recombination | Poly(ADP-ribose) | Homology | Genomes | Inactivation | Proteins | Ribose | Null cells | Deoxyribonucleic acid--DNA | BRCA2 protein | CRISPR | Deactivation | BRCA1 protein | Poly(ADP-ribose) polymerase | Adenosine diphosphate | Oligosaccharides | Double-strand break repair | Screens | Cisplatin | Inhibitors | Prostate | Viability | Tumors | Telomere-Binding Proteins / metabolism | Osteosarcoma / genetics | Telomere-Binding Proteins / genetics | BRCA1 Protein / genetics | Cellular Biology | Genetics | Proteins / genetics | Osteosarcoma / drug therapy | Ovarian Neoplasms / genetics | Mad2 Proteins / genetics | Proteins / metabolism | Breast Neoplasms / drug therapy | Breast Neoplasms / metabolism | Tumor Suppressor p53-Binding Protein 1 / genetics | BRCA1 Protein / deficiency | Ovarian Neoplasms / metabolism | Mad2 Proteins / metabolism | Breast Neoplasms / pathology | Bone Neoplasms / genetics | Ovarian Neoplasms / pathology | Bone Neoplasms / pathology | Life Sciences | Bone Neoplasms / drug therapy | Ovarian Neoplasms / drug therapy | Osteosarcoma / metabolism | Biochemistry, Molecular Biology | Breast Neoplasms / genetics | Drug Resistance, Neoplasm / genetics | Osteosarcoma / pathology | Bone Neoplasms / metabolism | Poly(ADP-ribose) Polymerase Inhibitors / pharmacology | Cisplatin / pharmacology | Molecular biology | Tumor Suppressor p53-Binding Protein 1 / metabolism | Cancer
Journal Article
American journal of human genetics, ISSN 0002-9297, 2016, Volume 99, Issue 5, pp. 1190 - 1198
.... To gain insights into its genetics, we performed whole-genome sequencing at very deep coverage of tumor-control pairs in 33 samples... 
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
Molecular cell, ISSN 1097-2765, 2016, Volume 64, Issue 1, pp. 51 - 64
Journal Article
Journal Article
Molecular cell, ISSN 1097-2765, 2017, Volume 65, Issue 4, pp. 671 - 684.e5
.... Resection-dependent c-NHEJ represents an inducible process during which Plk3 phosphorylates CtIP, mediating its interaction with Brca1 and promoting the initiation of resection... 
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
Molecular cell, ISSN 1097-2765, 2017, Volume 66, Issue 4, pp. 473 - 487.e9
The protein 53BP1 plays a central regulatory role in DNA double-strand break repair... 
RNF168 | RNF169 | 53BP1 | nucleosome | structural biology | NMR spectroscopy | biophysics | ubiquitylation | DNA repair | RAD18 | DEPENDENT SIGNALING CASCADE | STRUCTURAL BASIS | NMR-SPECTROSCOPY | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | X-RAY-SCATTERING | CLASS-SWITCH RECOMBINATION | RING FINGER | HOMOLOGOUS RECOMBINATION | DNA-DAMAGE-RESPONSE | CELL BIOLOGY | Multienzyme Complexes | Tumor Suppressor p53-Binding Protein 1 - chemistry | Humans | Ubiquitin - metabolism | Substrate Specificity | Structure-Activity Relationship | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | Ubiquitination | Nucleosomes - enzymology | Nuclear Magnetic Resonance, Biomolecular | Lysine - metabolism | Binding Sites | Tumor Suppressor p53-Binding Protein 1 - metabolism | Escherichia coli - enzymology | Tumor Suppressor p53-Binding Protein 1 - genetics | Enzyme Stability | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | Nucleosomes - genetics | Chromatin - pathology | DNA-Binding Proteins - genetics | Ubiquitin-Protein Ligases - chemistry | DNA-Binding Proteins - chemistry | Escherichia coli - genetics | DNA Repair | Protein Binding | Chromatin - enzymology | Protein Conformation | Nucleosomes - pathology | Histones - metabolism | Ubiquitin-Protein Ligases - genetics | Chromatin - genetics | Ubiquitin | Nuclear magnetic resonance spectroscopy | Chromatin | Molecular biology | Ligases
Journal Article
Nature (London), ISSN 1476-4687, 2017, Volume 543, Issue 7644, pp. 211 - 216
Journal Article
Journal Article