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Nature, ISSN 0028-0836, 2012, Volume 488, Issue 7413, pp. 665 - 669
LGR5+ stem cells reside at crypt bottoms, intermingled with Paneth cells that provide Wnt, Notch and epidermal growth factor signals. Here we find that the... 
IN-VITRO | INHIBITION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | UBIQUITYLATION | SMALL-INTESTINE | COLON | BETA-CATENIN | LGR5 | CANCER | NEGATIVE REGULATOR | Oncogene Proteins - genetics | Receptors, Wnt - antagonists & inhibitors | Cell Proliferation | Receptors, G-Protein-Coupled - metabolism | Humans | Ubiquitin - metabolism | Paneth Cells - pathology | Stem Cells - cytology | Receptors, Wnt - metabolism | Stem Cells - metabolism | DNA-Binding Proteins - deficiency | Adenoma - metabolism | DNA-Binding Proteins - metabolism | Endocytosis | Ubiquitination | Lysosomes - metabolism | Stem Cells - enzymology | Tumor Suppressor Proteins - deficiency | Organoids - metabolism | Tumor Suppressor Proteins - genetics | HEK293 Cells | Colorectal Neoplasms - metabolism | Paneth Cells - metabolism | Tumor Suppressor Proteins - metabolism | Organoids - pathology | Oncogene Proteins - metabolism | Organoids - cytology | Ubiquitin-Protein Ligases - metabolism | Frizzled Receptors - metabolism | DNA-Binding Proteins - genetics | beta Catenin - metabolism | Animals | Wnt Signaling Pathway - drug effects | Adenoma - pathology | Ubiquitin-Protein Ligases - deficiency | Oncogene Proteins - deficiency | Mice | Receptors, G-Protein-Coupled - genetics | Colorectal Neoplasms - pathology | Ubiquitin-Protein Ligases - genetics | Ubiquitin | Colorectal cancer | Physiological aspects | Development and progression | Research | Gene expression | Risk factors | Proteins | Epidermal growth factor | Mutation | Kinases | Rodents | Stem cells | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 512, Issue 1, pp. 49 - 53
Journal Article
Nature Cell Biology, ISSN 1465-7392, 05/2008, Volume 10, Issue 5, pp. 538 - 546
Journal Article
Science, ISSN 0036-8075, 10/2008, Volume 322, Issue 5901, pp. 597 - 602
Recent findings suggest important roles for nuclear organization in gene expression. In contrast, little is known about how nuclear organization contributes to... 
Yeasts | Medical research | Nuclear pore | DNA damage | Ubiquitins | DNA | Imaging | Genetic loci | Reports | DNA repair | Genetic mutation | ORGANIZATION | RECOMBINATION | REPAIR | REPLICATION | LIVING YEAST | MULTIDISCIPLINARY SCIENCES | DYNAMICS | DOUBLE-STRAND BREAKS | PROTEIN COMPLEXES | SACCHAROMYCES-CEREVISIAE | SUMOYLATION | Immunoprecipitation | DNA, Fungal - genetics | Saccharomyces cerevisiae - genetics | Intracellular Signaling Peptides and Proteins - metabolism | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | Nuclear Pore Complex Proteins - genetics | Saccharomyces cerevisiae - metabolism | Chromatin Immunoprecipitation | Recombination, Genetic | Genes, Fungal | Protein-Serine-Threonine Kinases - metabolism | Zinc Fingers | Nuclear Pore Complex Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Saccharomyces cerevisiae Proteins - genetics | DNA-Binding Proteins - genetics | Nuclear Pore - metabolism | Gene Conversion | Deoxyribonucleases, Type II Site-Specific - metabolism | DNA Repair | DNA, Fungal - metabolism | Saccharomyces cerevisiae Proteins - metabolism | Kinetics | Physiological aspects | Cellular proteins | Genetic aspects | Research | Ligases | Biomedical research | Yeast | Gene expression | Genomics | 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, 11/2009, Volume 36, Issue 3, pp. 457 - 468
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