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Journal of the American Chemical Society, ISSN 0002-7863, 08/2013, Volume 135, Issue 31, pp. 11623 - 11633
Journal Article
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2013, Volume 340, Issue 6136, pp. 1100 - 1106
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2009, Volume 119, Issue 12, pp. 3626 - 3636
The polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) is dysregulated in various cancers, and its upregulation strongly correlates... 
MEDICINE, RESEARCH & EXPERIMENTAL | BREAST-CANCER CELLS | DEVELOPMENTAL REGULATORS | CELLULAR MEMORY | E-CADHERIN EXPRESSION | HEMATOPOIETIC STEM-CELLS | PROSTATE-CANCER | MYC TRANSGENIC MICE | SELF-RENEWAL | NF-KAPPA-B | TRANSCRIPTION FACTOR | Nasopharyngeal Neoplasms - genetics | Neoplasm Transplantation | Nasopharyngeal Neoplasms - metabolism | Epithelial Cells - metabolism | Cadherins - metabolism | Humans | Glycogen Synthase Kinase 3 beta | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Mesoderm - cytology | Repressor Proteins - antagonists & inhibitors | Nasopharyngeal Neoplasms - pathology | Cadherins - genetics | Epithelial Cells - cytology | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Nasopharyngeal Neoplasms - etiology | Snail Family Transcription Factors | Nasopharynx - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | PTEN Phosphohydrolase - genetics | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Neoplasm Invasiveness | Down-Regulation | Gene Silencing | PTEN Phosphohydrolase - metabolism | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Animals | Polycomb Repressive Complex 1 | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mesoderm - metabolism | Mice | Nasopharynx - cytology | Chromatin | Care and treatment | Lymphomas | Research | Analysis | Cancer
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 2014, Volume 146, Issue 1, pp. 268 - 277.e18
... (MIR21, MIR23A, and MIR27A) that acted as cooperative repressors of a network of tumor suppressor genes that included PDCD4, BTG2, and NEDD4L... 
Gastroenterology and Hepatology | miRNA−mRNA Interaction | Tumorigenesis | Pancreatic Cancer | Oncogene | miRNA-mRNA Interaction | SURVIVAL | TRANSFORMATION | POSTTRANSCRIPTIONAL REGULATION | CANCER CELLS | DUCTAL ADENOCARCINOMA | NEDD4L | IN-VITRO | TARGETS | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | LASER MICRODISSECTION | Cell Proliferation | Prognosis | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Ubiquitin-Protein Ligases - antagonists & inhibitors | Gene Expression Profiling | Ubiquitin-Protein Ligases - physiology | Carcinoma, Pancreatic Ductal - genetics | Endosomal Sorting Complexes Required for Transport - antagonists & inhibitors | Genes, Tumor Suppressor - physiology | Nedd4 Ubiquitin Protein Ligases | Gene Expression Regulation, Neoplastic - genetics | RNA-Binding Proteins - antagonists & inhibitors | Immediate-Early Proteins - physiology | RNA-Binding Proteins - physiology | RNA, Messenger - genetics | Pancreatic Neoplasms - genetics | Disease Progression | Tumor Suppressor Proteins - physiology | Animals | Apoptosis Regulatory Proteins - antagonists & inhibitors | Cell Line, Tumor | Apoptosis Regulatory Proteins - physiology | Mice | MicroRNAs - genetics | MicroRNAs - physiology | Endosomal Sorting Complexes Required for Transport - physiology | Immediate-Early Proteins - antagonists & inhibitors | Care and treatment | MicroRNA | Pancreatic cancer | Analysis | Genes | Development and progression | Cancer
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2017, Volume 114, Issue 5, pp. 1027 - 1032
Journal Article
Nature (London), ISSN 0028-0836, 08/2009, Volume 460, Issue 7257, pp. 904 - 908
.... aUPD is associated not only with loss-of-function mutations of tumour suppressor genes... 
TRANSFORMATION | PROTEIN | RETROVIRAL VECTOR GCDNSAP | NEGATIVE REGULATION | MULTIDISCIPLINARY SCIENCES | HEMATOPOIETIC STEM-CELLS | V-CBL | MUTATIONS | UBIQUITIN LIGASES | MYELODYSPLASTIC SYNDROMES | P53 | NIH 3T3 Cells | Neoplasm Transplantation | ras Proteins - genetics | Phosphorylation | Proto-Oncogene Proteins c-cbl - metabolism | Humans | Leukemia, Myeloid - genetics | Molecular Sequence Data | ras Proteins - metabolism | Male | Leukemia, Myeloid - pathology | Allelic Imbalance | Ubiquitination | Base Sequence | Female | Proto-Oncogene Proteins c-cbl - deficiency | Genes, Tumor Suppressor | Proto-Oncogene Proteins c-cbl - genetics | Amino Acid Sequence | Oncogenes - genetics | Mutant Proteins - genetics | Models, Molecular | Mutant Proteins - metabolism | Chromosomes, Human, Pair 11 - genetics | Proto-Oncogene Proteins c-cbl - chemistry | Mice, Knockout | Animals | Uniparental Disomy - genetics | Leukemia, Myeloid - metabolism | Mice, Nude | Mutant Proteins - chemistry | Proto-Oncogene Proteins c-cbl - antagonists & inhibitors | Protein Conformation | Mice | Mutation | Gene mutations | Myelocytic leukemia | Physiological aspects | Tumor suppressor genes | Development and progression | Genetic aspects | Nonlymphoid leukemia | Research | Protein kinases | Proteins | Genes | Amino acids | Kinases | Cells | Clinical outcomes | Crystal structure | cytokine sensitivity | tumor suppressor | myelodysplasia | 490 | LOH | ubiquitination
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2017, Volume 292, Issue 37, pp. 15205 - 15215
... reactivation in cancer are not well-understood. Surprisingly, here we found occupancy of the metastasis suppressor non-metastatic 2 (NME2... 
CELLS | ACTIVATION | NM23-H2 | DNA | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | TRANSCRIPTION | GENE-EXPRESSION | HUMAN CANCERS | PROMOTER | GENOME | Epigenetic Repression | Humans | Protein Multimerization | Neoplasm Proteins - antagonists & inhibitors | Fibrosarcoma - metabolism | Neoplasm Proteins - metabolism | NM23 Nucleoside Diphosphate Kinases - genetics | NM23 Nucleoside Diphosphate Kinases - metabolism | Repressor Proteins - antagonists & inhibitors | Fibrosarcoma - pathology | Telomerase - genetics | Chromatin Immunoprecipitation | RNA Interference | Carcinoma - enzymology | G-Quadruplexes | Telomerase - metabolism | Carcinoma - pathology | Neoplasm Proteins - genetics | Genes, Reporter | Repressor Proteins - metabolism | Recombinant Proteins - metabolism | NM23 Nucleoside Diphosphate Kinases - chemistry | Promoter Regions, Genetic | Repressor Proteins - chemistry | Mutagenesis, Site-Directed | Histone Demethylases - chemistry | NM23 Nucleoside Diphosphate Kinases - antagonists & inhibitors | Cells, Cultured | Recombinant Proteins - chemistry | Repressor Proteins - genetics | Neoplasm Proteins - chemistry | Histone Demethylases - metabolism | Point Mutation | Cell Line, Tumor | Carcinoma - metabolism | Telomerase - antagonists & inhibitors | Fibrosarcoma - enzymology | Amino Acid Substitution | Gene Regulation | transcription regulation | chromatin modification | G-quadruplex | telomerase reverse transcriptase (TERT) | NME2 | REST repressor complex | epigenetics
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
In the presence of sustained DNA damage occurring in S-phase or G2, normal cells arrest before mitosis and eventually become senescent. The checkpoint kinases... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer | Life Sciences | Biochemistry, Molecular Biology
Journal Article
Oncogene, ISSN 0950-9232, 02/2008, Volume 27, Issue 7, pp. 997 - 1003
...Oncogene (2008) 27, 9971003 & 2008 Nature Publishing Group All rights reserved 0950-9232/08 $30.00 www.nature.com/onc ORIGINAL ARTICLE HDM2 antagonist Nutlin-3... 
HDM2 | Nutlin | p73 | Apoptosis | p53 | SITE | BIOCHEMISTRY & MOLECULAR BIOLOGY | apoptosis | MOLECULE MDM2 ANTAGONISTS | P53 PATHWAY | P63 | FAMILY | CELL BIOLOGY | ONCOLOGY | IN-VIVO | GENETICS & HEREDITY | SQUAMOUS-CELL CARCINOMA | MUTANT P53 | CENTRAL DOMAIN | Protein Biosynthesis | Immunoprecipitation | Humans | HCT116 Cells - metabolism | Immunoblotting | Bone Neoplasms - pathology | Tumor Suppressor Protein p53 - genetics | Bone Neoplasms - metabolism | DNA-Binding Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Transcription, Genetic | Bone Neoplasms - genetics | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Osteosarcoma - metabolism | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | RNA, Small Interfering - pharmacology | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Imidazoles - pharmacology | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Piperazines - pharmacology | Apoptosis Regulatory Proteins - metabolism | HCT116 Cells - pathology | Protein Binding | Apoptosis - physiology | Osteosarcoma - genetics | Causes of | Tumor suppressor genes | Genetic aspects | Research | Health aspects | Cancer | Oncology | Genetics | Inhibitor drugs | Binding sites
Journal Article
Oncogene, ISSN 1476-5594, 2007, Volume 26, Issue 32, pp. 4635 - 4647
...). APBs are PML bodies containing telomeric DNA and telomere-binding proteins, and are observed only in a small fraction of cells within asynchronously dividing ALT-positive cell populations... 
Telomeres | siRNA | Alternative lengthening of telomeres | Methionine restriction | PML | ALT-associated PML bodies | CANCER-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | telomeres | DNA-DAMAGE | MAMMALIAN-CELLS | PROTEIN COMPLEX | CELL BIOLOGY | HUMAN RAP1 | METABOLIC DEFECT | LARGE-BODY FORMATION | NUCLEAR-BODIES | ONCOLOGY | alternative lengthening of telomeres | methionine restriction | GENETICS & HEREDITY | PROMYELOCYTIC LEUKEMIA BODIES | TUMOR-CELL-LINES | Humans | Neoplasm Proteins - antagonists & inhibitors | Resting Phase, Cell Cycle | Autoantigens - genetics | RNA Interference | Neoplasm Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Telomeric Repeat Binding Protein 2 - antagonists & inhibitors | DNA Repair Enzymes - physiology | DNA-Binding Proteins - physiology | DNA-Binding Proteins - antagonists & inhibitors | Telomeric Repeat Binding Protein 2 - physiology | Genetic Techniques | Autoantigens - physiology | Tumor Suppressor Proteins - physiology | G1 Phase | Cell Line, Tumor | Intracellular Signaling Peptides and Proteins - physiology | Cell Cycle Proteins - physiology | Telomeric Repeat Binding Protein 1 - physiology | Tumor Suppressor Proteins - antagonists & inhibitors | Neoplasm Proteins - physiology | DNA Repair Enzymes - genetics | Telomeric Repeat Binding Protein 1 - genetics | Cell Cycle Proteins - antagonists & inhibitors | MRE11 Homologue Protein | Telomere-Binding Proteins - genetics | Tumor Suppressor Proteins - genetics | Telomere-Binding Proteins - physiology | Cell Cycle Proteins - genetics | Telomere - metabolism | DNA Repair Enzymes - antagonists & inhibitors | Nuclear Proteins - genetics | Methionine - deficiency | Telomere - genetics | Transcription Factors - physiology | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | RNA, Small Interfering - pharmacology | Antigens, Nuclear - physiology | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Telomere-Binding Proteins - antagonists & inhibitors | Antigens, Nuclear - genetics | Nuclear Proteins - antagonists & inhibitors | Telomeric Repeat Binding Protein 1 - antagonists & inhibitors | Cell Proliferation - drug effects | Nuclear Proteins - physiology | Telomeric Repeat Binding Protein 2 - genetics | Tumor Suppressor p53-Binding Protein 1 | Promyelocytic Leukemia Protein | Physiological aspects | Genetic aspects | Research | Cancer cells | Proteins | Ribonucleic acid | Cell cycle | Genetics | Oncology | Ribonucleic acid--RNA | DNA repair | Cancer
Journal Article