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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, 05/2006, Volume 441, Issue 7092, pp. 523 - 527
The proto-oncogene AKT (also known as PKB) is activated in many human cancers, mostly owing to loss of the PTEN tumour suppressor. In such tumours, AKT becomes... 
FORKHEAD TRANSCRIPTION FACTOR | APOPTOSIS | MULTIDISCIPLINARY SCIENCES | PROSTATE-CANCER | MUTATION | PTEN | MICE | FOXO3A | CELL-SURVIVAL | PML | PHOSPHATASES | Phosphorylation | Phosphoprotein Phosphatases - metabolism | Transcription Factors - deficiency | Neoplasm Proteins - metabolism | Cell Nucleus - enzymology | Tumor Suppressor Proteins - deficiency | Nuclear Proteins - deficiency | Tumor Suppressor Proteins - genetics | Female | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | PTEN Phosphohydrolase - genetics | PTEN Phosphohydrolase - deficiency | Tumor Suppressor Proteins - metabolism | Cells, Cultured | Nuclear Proteins - metabolism | Transcription Factors - genetics | Protein Transport | Transcription Factors - metabolism | Animals | Mice | Neoplasm Proteins - deficiency | Promyelocytic Leukemia Protein | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Membranes | Transcription factors | Inhibitor drugs | Pathogenesis | Oncology | AKT protein | Inactivation | Rodents | Cell cycle | Forkhead protein | Tumorigenesis | Null cells | FOXO3 protein | Phenotypes | Deactivation | Medical treatment | Cell membranes | Cell membranes (biology) | Sterility | Mutants | Cyclin-dependent kinase inhibitor p27 | Mutation | Prostate | PTEN protein | Tumors | Cancer | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 514, Issue 7521, pp. 247 - 251
The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types(1). However, loss-of-function mutations in PRC2 components occur in a... 
SUPPRESSOR | GENE | MULTIDISCIPLINARY SCIENCES | MICE | NF1 MICRODELETION PATIENTS | MUTATIONS | BET BROMODOMAIN INHIBITION | CANCER | TUMORS | NEUROFIBROMATOSIS TYPE-1 | EZH2 | Chromatin - metabolism | Transcription, Genetic - drug effects | Polycomb Repressive Complex 2 - genetics | Humans | Transcription Factors - deficiency | ras Proteins - metabolism | Neurofibromin 1 - deficiency | Glioma - genetics | Neoplasms - genetics | Melanoma - genetics | Tumor Suppressor Proteins - deficiency | Glioma - pathology | Nerve Sheath Neoplasms - pathology | Nuclear Proteins - deficiency | Tumor Suppressor Proteins - genetics | Epigenesis, Genetic - drug effects | Cell Death - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Nuclear Proteins - genetics | Chromatin - drug effects | Nerve Sheath Neoplasms - drug therapy | Disease Models, Animal | Triazoles - therapeutic use | Nerve Sheath Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | ras Proteins - antagonists & inhibitors | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Melanoma - pathology | Transcription Factors - genetics | Azepines - therapeutic use | Neoplasms - drug therapy | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Animals | Polycomb Repressive Complex 2 - deficiency | Melanoma - drug therapy | Nuclear Proteins - antagonists & inhibitors | Mice | Neoplasms - pathology | Polycomb Repressive Complex 2 - metabolism | Chromatin - genetics | Neurofibromin 1 - genetics | Glioma - drug therapy | Epigenetic inheritance | Ras genes | Genetic transcription | Research | Gliomas | Studies | Mutation | Genes | Tumors | Defects | Index Medicus
Journal Article
Nature Chemical Biology, ISSN 1552-4450, 2011, Volume 7, Issue 7, pp. 428 - 430
Journal Article
Science, ISSN 0036-8075, 12/2010, Volume 330, Issue 6009, pp. 1390 - 1393
Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in... 
T lymphocytes | Mitochondria | Cytokines | Thymocytes | Neurons | Cell death | REPORTS | Cytochromes | Mice | Potassium | Apoptosis | NEURONAL APOPTOSIS | CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | MECHANISM | MULTIDISCIPLINARY SCIENCES | BH3 DOMAINS | RELEASE | JNK PATHWAY | PROTEINS | BCL-2 FAMILY-MEMBERS | MEMBRANE PERMEABILIZATION | BH3 Interacting Domain Death Agonist Protein - deficiency | T-Lymphocytes - physiology | bcl-2-Associated X Protein - chemistry | Protein Multimerization | Stress, Physiological | bcl-2 Homologous Antagonist-Killer Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Membrane Proteins - deficiency | Caspases - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - deficiency | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Neurons - physiology | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Permeability | Proto-Oncogene Proteins - deficiency | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Cerebellum - cytology | Intracellular Membranes - metabolism | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Protein research | Genetic aspects | Mitochondrial DNA | Biochemical genetics | Research | Properties | Methods | Index Medicus
Journal Article
Cell Reports, ISSN 2211-1247, 05/2013, Volume 3, Issue 5, pp. 1339 - 1345
Journal Article
Nature Genetics, ISSN 1061-4036, 07/2012, Volume 44, Issue 7, pp. 751 - 759
Journal Article
Nature, ISSN 0028-0836, 11/2015, Volume 527, Issue 7576, pp. 100 - 104
Journal Article
Journal Article