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1. Full Text Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells
by Dev, Harveer and Chiang, Ting-Wei Will and Lescale, Chloe and de Krijger, Inge and Martin, Alistair G and Pilger, Domenic and Coates, Julia and Sczaniecka-Clift, Matylda and Wei, Wenming and Ostermaier, Matthias and Herzog, Mareike and Lam, Jonathan and Shea, Abigail and Demir, Mukerrem and Wu, Qian and Yang, Fengtang and Fu, Beiyuan and Lai, Zhongwu and Balmus, Gabriel and Belotserkovskaya, Rimma and Serra, Violeta and O’Connor, Mark J and Bruna, Alejandra and Beli, Petra and Pellegrini, Luca and Caldas, Carlos and Deriano, Ludovic and Jacobs, Jacqueline J. L and Galanty, Yaron and Jackson, Stephen P
Nature cell biology, ISSN 1465-7392, 08/2018, Volume 20, Issue 8, pp. 954 - 965
Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus | 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
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2. Full Text A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage response
by Adamson, Britt and Smogorzewska, Agata and Sigoillot, Frederic D and King, Randall W and Elledge, Stephen J
Nature cell biology, ISSN 1465-7392, 03/2012, Volume 14, Issue 3, pp. 318 - 328
Life Sciences & Biomedicine | Science & Technology | Cell Biology | RNA, Small Interfering - genetics | RNA-Binding Proteins - genetics | Histone Chaperones - genetics | Humans | Histone Chaperones - metabolism | Homologous Recombination | Immunoblotting | Green Fluorescent Proteins - genetics | Gene Regulatory Networks | Nuclear Pore Complex Proteins - genetics | RNA Interference | Cell Cycle Proteins - genetics | RNA Precursors - metabolism | Nuclear Proteins - genetics | Rad51 Recombinase - metabolism | Green Fluorescent Proteins - metabolism | Rad51 Recombinase - genetics | Nuclear Pore Complex Proteins - metabolism | Cell Cycle Proteins - metabolism | Heterogeneous-Nuclear Ribonucleoproteins - metabolism | Nuclear Proteins - metabolism | RNA Precursors - genetics | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Genome, Human - genetics | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Transcription Factors - metabolism | Poly(ADP-ribose) Polymerases - metabolism | BRCA2 Protein - metabolism | Poly(ADP-ribose) Polymerases - genetics | DNA Repair | Cell Line, Tumor | Models, Genetic | DNA Damage | BRCA2 Protein - genetics | Microscopy, Fluorescence | RNA-Binding Proteins - metabolism | Proteins | Physiological aspects | Research | Binding proteins | DNA damage | Ribonucleoproteins | Index Medicus
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3. Full Text A conserved NAD+ binding pocket that regulates protein-protein interactions during aging
by Li, Jun and Bonkowski, Michael S and Moniot, Sébastien and Zhang, Dapeng and Hubbard, Basil P and Ling, Alvin J.Y and Rajman, Luis A and Qin, Bo and Lou, Zhenkun and Gorbunova, Vera and Aravind, L and Steegborn, Clemens and Sinclair, David A
Science (American Association for the Advancement of Science), ISSN 0036-8075, 03/2017, Volume 355, Issue 6331, pp. 1312 - 1317
Adaptor Proteins, Signal Transducing - chemistry | Neoplasms - metabolism | RNA, Small Interfering - genetics | Humans | Aging - genetics | Neoplasms - genetics | HEK293 Cells | Conserved Sequence | DNA Damage - genetics | Protein Interaction Domains and Motifs | Paraquat - pharmacology | NAD - metabolism | Fibroblasts - metabolism | Models, Molecular | Radiation Tolerance - genetics | Poly (ADP-Ribose) Polymerase-1 - metabolism | Sequence Homology, Nucleic Acid | Animals | DNA Repair | Fibroblasts - drug effects | Adaptor Proteins, Signal Transducing - genetics | Poly (ADP-Ribose) Polymerase-1 - chemistry | Mice | Adaptor Proteins, Signal Transducing - metabolism | Poly (ADP-Ribose) Polymerase-1 - genetics | Aging - metabolism | DNA damage | Radiation | Homology | DNA repair | Proteins | Ribose | Aging | Inhibition | Supplementation | Repair | Damage accumulation | Age | Deoxyribonucleic acid--DNA | Binding | Adenosine | Adenine | Adenosine diphosphate | Abundance | Breast cancer | NAD | Poly(ADP-ribose) Polymerase 1 | Nicotinamide adenine dinucleotide | Nicotinamide | Protein interaction | Cancer | Index Medicus | Deoxyribonucleic acid | Breast
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4. Full Text Removal of Shelterin Reveals the Telomere End-Protection Problem
by Agnel Sfeir and Titia de Lange
Science (American Association for the Advancement of Science), ISSN 0036-8075, 5/2012, Volume 336, Issue 6081, pp. 593 - 597
Telomeres | Yeasts | Quantification | Lymphocytes | DNA | DNA damage | REPORTS | Cell cycle | Ataxia telangiectasia | Repression | Chromosomes | Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Fundamental and applied biological sciences. Psychology | Biological and medical sciences | Chromatin. Chromosome | Molecular and cellular biology | Molecular genetics | 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 | Index Medicus | Ataxia telangiectasia mutated protein
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5. Full Text DNA Repair Network Analysis Reveals Shieldin as a Key Regulator of NHEJ and PARP Inhibitor Sensitivity
by Gupta, Rajat and Somyajit, Kumar and Narita, Takeo and Maskey, Elina and Stanlie, Andre and Kremer, Magdalena and Typas, Dimitris and Lammers, Michael and Mailand, Niels and Nussenzweig, Andre and Lukas, Jiri and Choudhary, Chunaram
Cell (Cambridge), ISSN 0092-8674, 05/2018, Volume 173, Issue 4, pp. 972 - 988.e23
DNA damage repair | proximity labeling | shieldin | proteomics | 53BP1 | PARP inhibitors | telomere maintenance | antibody class-switch recombination | NHEJ | BRCA1 | Biochemistry & Molecular Biology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus
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6. Full Text Topoisomerase II beta interacts with cohesin and CTCF at topological domain borders
by Uusküla-Reimand, Liis and Hou, Huayun and Samavarchi-Tehrani, Payman and Rudan, Matteo Vietri and Liang, Minggao and Medina-Rivera, Alejandra and Mohammed, Hisham and Schmidt, Dominic and Schwalie, Petra and Young, Edwin J and Reimand, Jüri and Hadjur, Suzana and Gingras, Anne-Claude and Wilson, Michael D
Genome Biology, ISSN 1474-7596, 08/2016, Volume 17, Issue 1, pp. 182 - 182
BioID | DNA supercoiling | Genome organization | Hi-C | Proteomics | Topological associated domains | ChIP-seq | Comparative genomics | Topoisomerase II beta | Cohesin | CTCF | ChIP-exo | Genetics & Heredity | Life Sciences & Biomedicine | Biotechnology & Applied Microbiology | Science & Technology | Humans | DNA-Binding Proteins - metabolism | Poly-ADP-Ribose Binding Proteins | Chromatin Immunoprecipitation | Cell Cycle Proteins - genetics | Transcription, Genetic | Binding Sites | Chromosomes | Repressor Proteins - metabolism | DNA, Ribosomal - genetics | DNA Topoisomerases, Type II - metabolism | Promoter Regions, Genetic | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Repressor Proteins - genetics | DNA-Binding Proteins - genetics | Chromosomal Proteins, Non-Histone - genetics | Animals | Protein Interaction Maps - genetics | CCCTC-Binding Factor | Alleles | Protein Binding | DNA Topoisomerases, Type II - genetics | Mice | Genome | Chromatin - genetics | Deoxyribonuclease | DNA topoisomerase (ATP-hydrolysing) | Enzymes | Chromatin | Immunoprecipitation | Genomics | Genomes | Breast cancer | Regulatory sequences | Gene expression | Proteins | Nucleoli | Developmental stages | DNA methylation | Scientific imaging | Gene mapping | Protein interaction | Mass spectrometry | Bioinformatics | Deoxyribonucleic acid--DNA | Index Medicus | Research
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7. Full Text A GTPase-activating protein– binding protein (G3BP1)/antiviral protein relay conveys arteriosclerotic Wnt signals in aortic smooth muscle cells
by Ramachandran, Bindu and Stabley, John N and Cheng, Su-Li and Behrmann, Abraham S and Gay, Austin and Li, Li and Mead, Megan and Kozlitina, Julia and Lemoff, Andrew and Mirzaei, Hamid and Chen, Zhijian and Towler, Dwight A
The Journal of biological chemistry, ISSN 0021-9258, 2018, Volume 293, Issue 21, pp. 7942 - 7968
Life Sciences & Biomedicine | Biochemistry & Molecular Biology | Science & Technology | Calcinosis - genetics | RNA Helicases - metabolism | Poly-ADP-Ribose Binding Proteins - metabolism | Calcium - metabolism | Humans | Myocytes, Smooth Muscle - pathology | Antiviral Agents - metabolism | Aorta - metabolism | Arteriosclerosis - genetics | Wnt Proteins - metabolism | Wnt Proteins - genetics | RNA Helicases - genetics | Calcinosis - metabolism | RNA Recognition Motif Proteins - metabolism | DNA Helicases - genetics | Myocytes, Smooth Muscle - metabolism | Low Density Lipoprotein Receptor-Related Protein-6 | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Poly-ADP-Ribose Binding Proteins - genetics | beta Catenin - metabolism | beta Catenin - genetics | Mice, Knockout | Aorta - pathology | DNA Helicases - metabolism | Adaptor Proteins, Signal Transducing - physiology | Animals | Arteriosclerosis - metabolism | Mice | RNA Recognition Motif Proteins - genetics | Receptors, LDL - physiology | Calcinosis - pathology | Arteriosclerosis - pathology | Index Medicus | atherosclerosis | Type 2 diabetes | metabolic syndrome | Molecular Bases of Disease | cardiovascular disease | Wnt signaling | arteriosclerosis | protein methylation | vascular biology | calcification | vascular smooth muscle cells
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8. Full Text Immunogenic neoantigens derived from gene fusions stimulate T cell responses
by Yang, Wei and Lee, Ken-Wing and Srivastava, Raghvendra M and Kuo, Fengshen and Krishna, Chirag and Chowell, Diego and Makarov, Vladimir and Hoen, Douglas and Dalin, Martin G and Wexler, Leonard and Ghossein, Ronald and Katabi, Nora and Nadeem, Zaineb and Cohen, Marc A and Tian, S. Ken and Robine, Nicolas and Arora, Kanika and Geiger, Heather and Agius, Phaedra and Bouvier, Nancy and Huberman, Kety and Vanness, Katelynd and Havel, Jonathan J and Sims, Jennifer S and Samstein, Robert M and Mandal, Rajarsi and Tepe, Justin and Ganly, Ian and Ho, Alan L and Riaz, Nadeem and Wong, Richard J and Shukla, Neerav and Chan, Timothy A and Morris, Luc G. T and Sahlgrenska akademin and Institute of Clinical Sciences, Department of Pediatrics and Göteborgs universitet and Gothenburg University and Institutionen för kliniska vetenskaper, Avdelningen för pediatrik and Sahlgrenska Academy
Nature medicine, ISSN 1078-8956, 05/2019, Volume 25, Issue 5, pp. 767 - 775
Biochemistry & Molecular Biology | Life Sciences & Biomedicine | Medicine, Research & Experimental | Science & Technology | Cell Biology | Research & Experimental Medicine | Recombinant Fusion Proteins - immunology | Oncogene Proteins - genetics | Immunotherapy - methods | Humans | Proto-Oncogene Proteins c-myb - genetics | Programmed Cell Death 1 Receptor - antagonists & inhibitors | NFI Transcription Factors - genetics | Squamous Cell Carcinoma of Head and Neck - immunology | Neoplasms - therapy | Neoplasms - genetics | Nuclear Proteins - genetics | Oncogene Proteins - immunology | T-Lymphocytes, Cytotoxic - immunology | Antigens, Neoplasm - genetics | Head and Neck Neoplasms - therapy | Poly-ADP-Ribose Binding Proteins - genetics | Gene Fusion | Proto-Oncogene Proteins c-myb - immunology | Nuclear Proteins - immunology | Chromosomal Proteins, Non-Histone - genetics | Whole Genome Sequencing | Chromosomal Proteins, Non-Histone - immunology | Head and Neck Neoplasms - immunology | Squamous Cell Carcinoma of Head and Neck - genetics | Neoplasms - immunology | Recombinant Fusion Proteins - genetics | Head and Neck Neoplasms - genetics | Poly-ADP-Ribose Binding Proteins - immunology | Squamous Cell Carcinoma of Head and Neck - therapy | NFI Transcription Factors - immunology | Care and treatment | Immune response | Patient outcomes | Immunotherapy | Tumor antigens | Head and neck cancer | Genetic aspects | T cells | Identification and classification | Health aspects | Gene fusion | Antigens | Cytotoxicity | Immunosurveillance | Genomes | Lymphocytes T | Ribonucleic acid--RNA | Immunity | Metastases | Gene sequencing | Inhibitors | Immune checkpoint | Immunogenicity | Lymphocytes | Antigen (tumor-associated) | Infiltration | Mutation | Pretreatment | Tumors | Cancer | Index Medicus | tumor-antigens | somatic mutations | bcr-abl | induction | blockade | immunotherapy | protein | peptides | cancer | Cancer and Oncology | landscape | Cancer och onkologi
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