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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 | Metastasis | Pathogenesis | Genomics | Deoxyribonucleic acid--DNA | Index Medicus | Report
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 | Index Medicus
Journal Article
Journal Article
Nature Structural and Molecular Biology, ISSN 1545-9993, 07/2016, Volume 23, Issue 7, pp. 647 - 655
The opposing activities of 53BP1 and BRCA1 influence pathway choice in DNA double-strand-break repair. How BRCA1 counteracts the inhibitory effect of 53BP1 on... 
STRAND BREAK REPAIR | RING-RING COMPLEX | TUMOR SUPPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | REPAIR PATHWAY CHOICE | BRCA1 | REMODELING ENZYME | CELL BIOLOGY | E3 LIGASE | BIOPHYSICS | END RESECTION | HOMOLOGOUS RECOMBINATION | FUN30 | Chromatin - metabolism | DNA, Neoplasm - metabolism | Humans | Gene Expression Regulation, Neoplastic | Ubiquitin - metabolism | DNA Breaks, Double-Stranded | Ubiquitination - drug effects | BRCA1 Protein - metabolism | Tumor Suppressor Proteins - genetics | Cloning, Molecular | Escherichia coli - metabolism | Binding Sites | Chromatin - drug effects | DNA Helicases - genetics | Chromatin - chemistry | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinant Proteins - metabolism | Gene Expression | Recombinational DNA Repair | Tumor Suppressor Proteins - metabolism | Tumor Suppressor p53-Binding Protein 1 - genetics | Signal Transduction | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | Recombinant Proteins - genetics | Ubiquitin - genetics | Piperazines - pharmacology | DNA Cleavage - drug effects | BRCA1 Protein - genetics | DNA Helicases - metabolism | Phthalazines - pharmacology | Histones - genetics | Escherichia coli - genetics | Protein Binding | DNA, Neoplasm - genetics | HeLa Cells | Histones - metabolism | Ubiquitin-Protein Ligases - genetics | Camptothecin - pharmacology | Breast cancer | BRCA mutations | DNA repair | Analysis | Risk factors | Enzymes | Protein expression | Chromatin | DNA damage | Index Medicus
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 | Index Medicus
Journal Article
Molecular Cell, ISSN 1097-2765, 05/2016, Volume 62, Issue 3, pp. 409 - 421
Journal Article
Molecular Cell, ISSN 1097-2765, 05/2017, Volume 66, Issue 4, pp. 473 - 487.e9
The protein 53BP1 plays a central regulatory role in DNA double-strand break repair. 53BP1 relocates to chromatin by recognizing RNF168-mediated... 
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 | Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 08/2018, 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. To... 
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 | 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 | 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 | ADP | Proteins | Ribose | Null cells | Deoxyribonucleic acid--DNA | BRCA2 protein | CRISPR | Deactivation | BRCA1 protein | Poly(ADP-ribose) polymerase | Oligosaccharides | Double-strand break repair | Screens | Cisplatin | Polymerase | Inhibitors | Breast | Prostate | Viability | Tumors | Cancer | Index Medicus
Journal Article
Journal Article
Oncogene, ISSN 0950-9232, 04/2017, Volume 36, Issue 17, pp. 2405 - 2422
Journal Article
Nature Biotechnology, ISSN 1087-0156, 01/2018, Volume 36, Issue 1, pp. 95 - 102
Journal Article