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Nature cell biology, ISSN 1476-4679, 2018, Volume 20, Issue 8, pp. 954 - 965
.... We identified two previously uncharacterized proteins, C2Oorf196 and FAM35A, whose inactivation confers strong PARP-inhibitor resistance... 
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 | Polymerase | 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
Nature communications, ISSN 2041-1723, 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 | Comparative analysis | Species | PTEN protein | Tumors
Journal Article
Biochemical Journal, ISSN 0264-6021, 01/2012, Volume 441, Issue 2, pp. 523 - 540
...) proteins and 50 lysosomal hydrolases. Autophagosomes... 
Mitochondrion | Oxidative stress | Redox signalling | Neurodegeneration | Autophagy | Nitrative stress | autophagy | CHAPERONE-MEDIATED AUTOPHAGY | ANTIOXIDANT RESPONSIVE ELEMENTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIPOFUSCINOSES BATTEN-DISEASE | neurodegeneration | AMYOTROPHIC-LATERAL-SCLEROSIS | mitochondrion | redox signalling | MOTOR-NEURON DEGENERATION | MANGANESE SUPEROXIDE-DISMUTASE | nitrative stress | SMOOTH-MUSCLE-CELLS | PATHOGENIC DJ-1 MUTATIONS | HYPOXIA-INDUCED AUTOPHAGY | oxidative stress | COMPLEX-I DEFICIENCY | Protein Kinases - metabolism | Transcription, Genetic - drug effects | Cardiovascular Diseases - physiopathology | Reactive Oxygen Species - metabolism | Oxidation-Reduction | Reactive Nitrogen Species - metabolism | Humans | Oxidative Stress - physiology | Hydrogen Peroxide - pharmacology | Oncogene Proteins - metabolism | Nitric Oxide - physiology | Autophagy - physiology | Intracellular Signaling Peptides and Proteins - metabolism | Mitochondria - metabolism | Mitochondria - pathology | Parkinson Disease - physiopathology | Lysosomes - physiology | Protein Deglycase DJ-1 | Animals | Signal Transduction - physiology | TOR Serine-Threonine Kinases - physiology | Neoplasms - physiopathology | AMPK, 5′-AMP-activated protein kinase | NBR1, neighbour of BRCA1 (breast cancer early-onset 1) | NGF, nerve growth factor | LC3, light chain 3 | NOX, NADPH oxidase | EM, electron microscopy | TOR, target of rapamycin | ULK, unc (unco-ordinated family member)-51-like kinase | mtDNA, mitochondrial DNA | mTOR, mammalian target of rapamycin | IKKβ, IκB kinase β | LRRK2, leucine-rich repeat kinase 2 | NAC, N-acetyl-L-cysteine | Nrf2, nuclear factor-erythroid 2-related factor 2 | PI3P, phosphatidylinositol 3-phosphate | ECH, enoyl-CoA hydratase | BNIP3L, BNIP3-like | Drp1, dynamin-related protein 1 | tfLC3, tandem fluorescently tagged LC3 | NF-κB, nuclear factor κB | BAG, Bcl-2-associated athanogene | Keap1, Kelch-like ECH-associated protein 1 | PE, phosphatidylethanolamine | 3-MA, 3-methyladenine | UCP, uncoupling protein | IκB, inhibitor of nuclear factor κB | FIP200, focal adhesion kinase family-interacting protein of 200 kDa | PI3K, phosphoinositide 3-kinase | HNE, 4-hydroxynonenal | Review | ALS, amyotrophic lateral sclerosis | ATG, AuTophaGy-related | adenovirus E18 19-kDa-interacting protein | Tzb, trastuzumab | mETC, mitochondrial electron-transport chain | Rubicon, RUN domain- and cysteine-rich domain-containing beclin-1-interacting protein | VDAC, voltage-dependent anion channel | IP3, inositol 1,4,5-trisphosphate | RFP, red fluorescent protein | ROS, reactive oxygen species | TNFα, tumour necrosis factor α | PINK1, PTEN (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1 | GFP, green fluorescent protein | LAMP, lysosome-associated membrane protein | JNK1, c-Jun N-terminal kinase 1 | TAC, transverse aortic constriction | GABARAP, GABAA (γ-aminobutyric acid type A)-receptor-associated protein | HIF-1, hypoxia-inducible factor 1 | NOS, nitric oxide synthase | siRNA, small interfering RNA | SOD, superoxide dismutase | RLS, reactive lipid species | RNS, reactive nitrogen species | ER, endoplasmic reticulum | TIGAR, TP53 (tumour protein 53)-induced glycolysis and apoptosis regulator | Vps34, vacuolar protein sorting 34 | BNIP, Bcl-2
Journal Article
Nature communications, ISSN 2041-1723, 2018, Volume 9, Issue 1, pp. 2280 - 14
Defects in DNA repair can cause various genetic diseases with severe pathological phenotypes. Fanconi anemia ( FA) is a rare disease characterized by bone... 
UBIQUITINATION | DAMAGE RESPONSE | CHROMATIN | CROSS-LINK REPAIR | HUMAN-CELLS | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | BRCA1 | ENRICHMENT ANALYSIS | ASSOCIATION | NUCLEASE | Genetic Therapy | Ubiquitin-Specific Proteases - genetics | Fanconi Anemia Complementation Group D2 Protein - genetics | Fanconi Anemia - metabolism | Humans | DNA Repair - physiology | DNA Repair - genetics | Fanconi Anemia Complementation Group C Protein - genetics | Fanconi Anemia Complementation Group A Protein - genetics | Fanconi Anemia Complementation Group D2 Protein - deficiency | Fanconi Anemia Complementation Group A Protein - metabolism | Fanconi Anemia Complementation Group Proteins - metabolism | Ubiquitination | Fanconi Anemia Complementation Group G Protein - genetics | Ubiquitin-Specific Proteases - deficiency | Fanconi Anemia Complementation Group G Protein - deficiency | BRCA1 Protein - metabolism | Fanconi Anemia - genetics | Ubiquitin-Specific Proteases - metabolism | Chromosomal Instability | Rad51 Recombinase - metabolism | Cell Line | Fanconi Anemia Complementation Group Proteins - deficiency | Fanconi Anemia Complementation Group Proteins - genetics | Fanconi Anemia Complementation Group G Protein - metabolism | Gene Knockout Techniques | Fanconi Anemia Complementation Group C Protein - metabolism | Fanconi Anemia Complementation Group D2 Protein - metabolism | Fanconi Anemia Complementation Group A Protein - deficiency | CRISPR-Cas Systems | Fanconi Anemia Complementation Group C Protein - deficiency | Fanconi Anemia - therapy | DNA Damage | Histones - metabolism | Mutation
Journal Article
Cancer cell, ISSN 1535-6108, 2007, Volume 11, Issue 2, pp. 103 - 105
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
Molecular & cellular proteomics, ISSN 1535-9484, 2015, Volume 14, Issue 5, pp. 1419 - 1434
.... Small Ubiquitin-like Modifiers (SUMOs) are known to counteract replication stress, nevertheless, only a small number of relevant SUMO target proteins are known... 
E3 LIGASE | PCNA | PATHWAY | HUMAN-CELLS | BIOCHEMICAL RESEARCH METHODS | REQUIRES | SUMO-1 CONJUGATION | NEDD8-ACTIVATING ENZYME | DNA-REPAIR | IDENTIFICATION | SIGNALING NETWORKS | Adaptor Proteins, Signal Transducing - chemistry | Genomic Instability | Hydroxyurea - pharmacology | Nucleic Acid Synthesis Inhibitors - pharmacology | Humans | Molecular Sequence Data | Chromatin Assembly Factor-1 - metabolism | Trans-Activators - chemistry | Recombinant Fusion Proteins - metabolism | DNA-Binding Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - genetics | BRCA1 Protein - metabolism | Chromatin Assembly Factor-1 - genetics | Endodeoxyribonucleases - metabolism | Trans-Activators - genetics | Carrier Proteins - chemistry | Lysine - metabolism | Osteoblasts - cytology | Nuclear Proteins - genetics | BRCA1 Protein - chemistry | Amino Acid Sequence | Gene Expression | Signal Transduction | Chromatin Assembly Factor-1 - chemistry | Small Ubiquitin-Related Modifier Proteins - metabolism | Osteoblasts - drug effects | DNA Replication | Nuclear Proteins - metabolism | Endodeoxyribonucleases - chemistry | Recombinant Fusion Proteins - chemistry | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Protein Interaction Mapping | BRCA1 Protein - genetics | Carrier Proteins - genetics | Endodeoxyribonucleases - genetics | Carrier Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - chemistry | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Recombinant Fusion Proteins - genetics | Sumoylation | Trans-Activators - metabolism | DNA Damage | Adaptor Proteins, Signal Transducing - metabolism | Lysine - chemistry | Osteoblasts - metabolism | Technological Innovation and Resources
Journal Article
The EMBO Journal, ISSN 0261-4189, 02/2010, Volume 29, Issue 3, pp. 574 - 585
The Mre11/Rad50/Nbs1 (MRN) complex has a central function in facilitating activation of the ATM protein kinase at sites of DNA double‐strand breaks (DSBs... 
MRN | checkpoints | ATM | DNA repair | 53BP1 | Checkpoints | DEPENDENT PHOSPHORYLATION | MRE11 COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | TELANGIECTASIA-LIKE DISORDER | S-PHASE CHECKPOINT | CELL BIOLOGY | BRCT PROTEIN 53BP1 | CLASS-SWITCH RECOMBINATION | DNA-DAMAGE-RESPONSE | ATAXIA-TELANGIECTASIA | IONIZING IRRADIATION | Phosphorylation | Protein Binding - genetics | Humans | Recombinant Fusion Proteins - physiology | Multiprotein Complexes - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Recombinant Fusion Proteins - metabolism | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Multiprotein Complexes - metabolism | BRCA1 Protein - metabolism | DNA Repair Enzymes - metabolism | Protein Multimerization - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | DNA-Binding Proteins - physiology | Tumor Suppressor Proteins - metabolism | Protein-Serine-Threonine Kinases - physiology | Cell Cycle Proteins - metabolism | Cells, Cultured | Nuclear Proteins - metabolism | Protein Structure, Tertiary - genetics | Ataxia Telangiectasia Mutated Proteins | Multiprotein Complexes - physiology | Tumor Suppressor Proteins - physiology | Animals | Recombinant Fusion Proteins - genetics | Mice | Tumor Suppressor p53-Binding Protein 1 | Enzyme Activation - genetics | Intracellular Signaling Peptides and Proteins - physiology | Cell Cycle Proteins - physiology | Protein Structure, Tertiary - physiology | Signal transduction | Kinases | Molecular biology | Substrates
Journal Article