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Nature Communications, ISSN 2041-1723, 12/2019, Volume 10, Issue 1, pp. 353 - 14
Mucosal melanoma is a rare and poorly characterized subtype of human melanoma. Here we perform a cross-species analysis by sequencing tumor-germline pairs from... 
POINT MUTATIONS | CANCER PATIENTS | BREAST-CANCER | MUTATIONAL PROCESSES | ARRAY-CGH | MULTIDISCIPLINARY SCIENCES | COPY NUMBER | TUMOR | OVARIAN-CANCER | MOUSE MODELS | REVEALS | Proto-Oncogene Proteins c-mdm2 - genetics | Cadherins - metabolism | Humans | Carcinogenesis - metabolism | DNA Copy Number Variations | Germ-Line Mutation | Cadherins - genetics | Neoplasm Proteins - genetics | Mouth Neoplasms - genetics | Protein-Serine-Threonine Kinases - metabolism | PTEN Phosphohydrolase - genetics | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Carcinogenesis - genetics | Cell Cycle Proteins - metabolism | Melanoma - pathology | Mucous Membrane - pathology | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Microtubule-Associated Proteins - genetics | Species Specificity | Microtubule-Associated Proteins - metabolism | Gene Expression Regulation, Neoplastic | Mouth Neoplasms - metabolism | Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics | Neoplasm Proteins - metabolism | Tumor Suppressor Protein p53 - genetics | Melanoma - genetics | BRCA1 Protein - metabolism | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Membrane Proteins - metabolism | Proto-Oncogene Proteins c-mdm2 - metabolism | Melanoma - metabolism | Skin Neoplasms - pathology | Neoplasm Recurrence, Local | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | PTEN Phosphohydrolase - metabolism | Mucous Membrane - metabolism | Skin Neoplasms - metabolism | Carcinogenesis - pathology | BRCA1 Protein - genetics | Animals | BRCA2 Protein - metabolism | Receptor-Like Protein Tyrosine Phosphatases, Class 3 - metabolism | Skin Neoplasms - genetics | Dogs | Horses | Mouth Neoplasms - pathology | BRCA2 Protein - genetics | BRCA2 protein | MDM2 protein | BRCA1 protein | Copy number | p53 Protein | Mucosa | Melanoma | Data processing | Breast cancer | Metastases | Heterogeneity | Human performance | Tumorigenesis | Mutation | Species | PTEN protein | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 12/2015, Volume 528, Issue 7582, pp. 422 - 426
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 | Index Medicus | RNF168 | Brca1 | genomic stability | telomere | ATM | NHEJ
Journal Article
Nature, ISSN 0028-0836, 2015, Volume 521, Issue 7553, pp. 541 - U308
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 07/2012, Volume 109, Issue 27, pp. E1839 - E1847
In the course of apoptosis, activated caspases cleave ∼500 to ∼1,000 different proteins in a mammalian cell. The dynamics of apoptosis involve a number of... 
ATE1 | Arginylation | UBR1 | Proteolysis | APOPTOSIS | ACTIVATION | UBIQUITIN LIGASE | MULTIDISCIPLINARY SCIENCES | KAPPA-B | DEGRADATION SIGNALS | CANCER | arginylation | CASPASES | RIP | proteolysis | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Humans | Aminoacyltransferases - genetics | Caspase 3 - metabolism | bcl-X Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | Phosphoproteins - metabolism | Lim Kinases - metabolism | Mice, Mutant Strains | BRCA1 Protein - metabolism | HEK293 Cells | Antibodies - immunology | Apoptosis Regulatory Proteins - genetics | Peptide Fragments - genetics | BH3 Interacting Domain Death Agonist Protein - metabolism | Rabbits | Peptide Fragments - metabolism | TNF Receptor-Associated Factor 1 - metabolism | Ubiquitin-Protein Ligases - metabolism | TNF Receptor-Associated Factor 1 - genetics | Phosphoproteins - genetics | Apoptosis Regulatory Proteins - metabolism | BRCA1 Protein - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Adaptor Proteins, Signal Transducing - genetics | Lim Kinases - genetics | Aminoacyltransferases - metabolism | Mice | Apoptosis - physiology | Adaptor Proteins, Signal Transducing - metabolism | Ubiquitin-Protein Ligases - genetics | bcl-X Protein - metabolism | Arginine - metabolism | Proteins | Mutation | Metabolism | Proteases | Apoptosis | Index Medicus | Biological Sciences | PNAS Plus
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
Cancer Cell, ISSN 1535-6108, 2007, Volume 11, Issue 2, pp. 103 - 105
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
Journal Article
Science, ISSN 0036-8075, 12/2007, Volume 318, Issue 5856, pp. 1637 - 1640
Cells respond to DNA double-strand breaks by recruiting factors such as the DNA-damage mediator protein MDC1, the p53-binding protein 1 (53BP1), and the breast... 
Phosphorylation | Ubiquitins | DNA damage | DNA | Cell lines | HeLa cells | Small interfering RNA | Antibodies | Irradiation | Reports | Mice | MDC1 | RECOGNITION | 53BP1 | MULTIDISCIPLINARY SCIENCES | DOUBLE-STRAND BREAKS | NUCLEAR FOCI | HISTONE H2AX | ATM | CHECKPOINT | BRCA1 | CELLULAR-RESPONSE | Humans | Ubiquitin - metabolism | Molecular Sequence Data | Intracellular Signaling Peptides and Proteins - metabolism | Trans-Activators - chemistry | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | Ubiquitination | BRCA1 Protein - metabolism | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Amino Acid Sequence | Tumor Suppressor Proteins - metabolism | Cell Nucleus Structures - genetics | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Amino Acid Motifs | Ubiquitin-Conjugating Enzymes - metabolism | DNA Repair | Cell Line, Tumor | Trans-Activators - metabolism | RNA, Small Interfering | HeLa Cells | Tumor Suppressor p53-Binding Protein 1 | Ubiquitin | Physiological aspects | Genetic aspects | Proteins | Enzymes | Cellular biology | Deoxyribonucleic acid | Breast cancer | Mutation | Kinases | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 12/2009, Volume 462, Issue 7275, pp. 935 - 939
Journal Article