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Genes and Development, ISSN 0890-9369, 01/2007, Volume 21, Issue 1, pp. 43 - 48
Here we report that RNA interference against ATM inhibited p53 accumulation in cells expressing oncogenic STAT5 and cooperated with Rb inactivation to suppress... 
Senescence | DNA damage | E2F1 | STAT5 | ATM | RasV12 | p53 | ACTIVATION | P19(ARF) | RAS | PHOSPHORYLATION | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | senescence | PREMATURE SENESCENCE | IN-VIVO | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | HUMAN FIBROBLASTS | CHECKPOINT | Protein Kinases - metabolism | Phosphorylation | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Oncogenes - physiology | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Genes, ras - physiology | STAT5 Transcription Factor - metabolism | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | RNA, Small Interfering - pharmacology | Retinoblastoma Protein - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cellular Senescence - physiology | Ataxia Telangiectasia Mutated Proteins | E2F1 Transcription Factor - metabolism | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic | Fluorescent Antibody Technique | Retinoblastoma Protein - antagonists & inhibitors | Checkpoint Kinase 2 | Checkpoint Kinase 1 | Fibroblasts - cytology | DNA Damage | Mutation | Aging | Genetic research | Research | Index Medicus | Research Communication
Journal Article
Molecular Cell, ISSN 1097-2765, 2001, Volume 7, Issue 5, pp. 915 - 926
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2008, Volume 118, Issue 1, pp. 79 - 88
Despite great interest in cancer chemoprevention, effective agents are few. Here we show that chloroquine, a drug that activates the stress-responsive Atm-p53... 
MEDICINE, RESEARCH & EXPERIMENTAL | BCL-X-L | SIGNALING PATHWAYS | INDUCED APOPTOSIS | PHOSPHORYLATION | ATM | AUTOPHAGY | CYTOCHROME-C RELEASE | MYC-INDUCED LYMPHOMAGENESIS | TRANSGENIC MICE | P53 | Apoptosis - drug effects | Humans | Apoptosis - genetics | Male | Autophagy - drug effects | Burkitt Lymphoma - pathology | Neoplasms, Experimental - pathology | Chloroquine - pharmacology | Cell Transformation, Neoplastic - genetics | Autophagy - genetics | B-Lymphocytes - pathology | B-Lymphocytes - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | Embryo, Mammalian - pathology | Cell Cycle Proteins - metabolism | Neoplasms, Experimental - prevention & control | bcl-2-Associated X Protein - metabolism | Ataxia Telangiectasia Mutated Proteins | Fibroblasts - pathology | Ataxia Telangiectasia - pathology | Ataxia Telangiectasia - genetics | Mice | Proto-Oncogene Proteins c-myc - genetics | Neoplasms, Experimental - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Embryo, Mammalian - metabolism | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Caspases - metabolism | Lysosomes - metabolism | Burkitt Lymphoma - prevention & control | Mice, Mutant Strains | Tumor Suppressor Proteins - genetics | Neoplasms, Experimental - genetics | Burkitt Lymphoma - genetics | Cell Cycle Proteins - genetics | Female | Lysosomes - pathology | Antirheumatic Agents - pharmacology | bcl-2-Associated X Protein - genetics | Antirheumatic Agents - therapeutic use | Ataxia Telangiectasia - prevention & control | Caspases - genetics | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Burkitt Lymphoma - metabolism | Chloroquine - therapeutic use | Ataxia Telangiectasia - metabolism | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Animals | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Cell Transformation, Neoplastic - pathology | Prevention | Chloroquine | Lysosomes | Dosage and administration | Research | Drug therapy | Health aspects | Cancer | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2004, Volume 279, Issue 9, pp. 8076 - 8083
Journal Article
Journal Article
Nanoscale, ISSN 2040-3364, 09/2018, Volume 10, Issue 36, pp. 17227 - 17235
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2014, Volume 111, Issue 43, pp. 15532 - 15537
X-linked inhibitor of apoptosis (XIAP)-associated factor 1 (XAF1) is a tumor suppressor that is frequently inactivated in many human cancers. However, the... 
Phosphorylation | HCT116 cells | Ubiquitins | Control loops | Cell lines | Gene expression regulation | Mathematical functions | Tumors | Apoptosis | Cancer | XAF1 | ZNF313 | Siah2 | HIPK2 | P53 | CANCER-CELLS | DOMAIN | HYPERMETHYLATION | X-LINKED INHIBITOR | MULTIDISCIPLINARY SCIENCES | INTERACTING PROTEIN KINASE-2 | IDENTIFICATION | p53 | GENE | XIAP-ASSOCIATED FACTOR-1 | PROSTATE-CANCER | EXPRESSION | Neoplasms - metabolism | Apoptosis - drug effects | Humans | Antineoplastic Agents - therapeutic use | Intracellular Signaling Peptides and Proteins - metabolism | Neoplasm Proteins - metabolism | Proteolysis - drug effects | Protein Isoforms - metabolism | Ubiquitination - drug effects | Protein Binding - drug effects | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Proto-Oncogene Proteins c-mdm2 - metabolism | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | HCT116 Cells | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Neoplasm Proteins - chemistry | Nuclear Proteins - metabolism | Enzyme Activation - drug effects | Phosphoserine - metabolism | Remission Induction | Neoplasms - drug therapy | Carrier Proteins - metabolism | Signal Transduction - drug effects | Intracellular Signaling Peptides and Proteins - chemistry | Models, Biological | Protein Stability - drug effects | Feedback, Physiological - drug effects | Tumor Suppressor Protein p53 - chemistry | Neoplasms - pathology | Physiological aspects | Physiological research | Research | Zinc finger proteins | Tumor proteins | Protein kinases | Proteins | Cell cycle | Index Medicus | Biological Sciences
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 9, pp. e73875 - e73875
Excessive reactive oxygen species (ROS) induce apoptosis and are associated with various diseases and with aging. SIRT1 (sirtuin-1), an NAD+-dependent protein... 
TRANSCRIPTION FACTORS | HEART | HSIR2(SIRT1) | RESVERATROL | PROMOTES CELL-SURVIVAL | ACTIVATION | DEACETYLASE | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | MUSCULAR-DYSTROPHY | EXPRESSION | Sirtuin 1 - metabolism | AMP-Activated Protein Kinases - metabolism | Superoxide Dismutase - genetics | Cell Proliferation | Reactive Oxygen Species - metabolism | Oxidative Stress | Apoptosis - drug effects | Humans | Apoptosis - genetics | Stilbenes - pharmacology | Sirtuin 1 - genetics | Antimycin A - pharmacology | Tumor Suppressor Protein p53 - genetics | Gene Knockdown Techniques | Forkhead Transcription Factors - metabolism | Superoxide Dismutase - metabolism | Cell Line | Hydrogen Peroxide - pharmacology | Tumor Suppressor Protein p53 - metabolism | Enzyme Activation - drug effects | Forkhead Transcription Factors - genetics | Hydrogen Peroxide - metabolism | Animals | Forkhead Box Protein O1 | Mice | Forkhead Box Protein O3 | Niacinamide | Oxidative stress | Ionizing radiation | Resveratrol | DNA binding proteins | Tumor proteins | Apoptosis | NADPH | Transcription factors | p53 Protein | Superoxide dismutase | Kinases | Modulators | Muscular dystrophy | Proteins | Mitochondria | FOXO1 protein | Rodents | Antimycin A | Aging | FOXO4 protein | Forkhead protein | FOXO3 protein | Heart failure | Stresses | Immunoglobulins | Cell survival | Pharmacology | siRNA | Survival | SIRT1 protein | Stress | NAD | Medicine | Deacetylation | Cell death | Tumor suppressor genes | Nicotinamide | Mutation | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, pp. e75483 - e75483
Ras association domain family protein 1A (RASSF1A) is a tumor suppressor gene silenced in cancer. Here we report that RASSF1A is a novel regulator of... 
YES-ASSOCIATED PROTEIN | APOPTOSIS | C-ABL | DNA METHYLTRANSFERASE-1 | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | YAP | STEM-CELL PROLIFERATION | NF-KAPPA-B | PROMOTES | P53 | Inflammation - pathology | Apoptosis - drug effects | Colitis, Ulcerative - genetics | Colon - drug effects | NF-kappa B - metabolism | Intestinal Mucosa - drug effects | Tumor Suppressor Proteins - deficiency | Colitis, Ulcerative - drug therapy | Toll-Like Receptors - metabolism | Tumor Suppressor Proteins - metabolism | Signal Transduction | Colon - pathology | bcl-2-Associated X Protein - metabolism | Epithelial Cells - pathology | Colitis, Ulcerative - pathology | Pyrimidines - pharmacology | Piperazines - pharmacology | Colon - metabolism | Mice, Knockout | Tumor Protein p73 | Toll-Like Receptors - genetics | Mice | Intestinal Mucosa - pathology | Inflammation - chemically induced | Dextran Sulfate | Intestinal Mucosa - metabolism | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Phosphoproteins - metabolism | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Inflammation - drug therapy | Tumor Suppressor Proteins - genetics | Benzamides - pharmacology | Nuclear Proteins - genetics | bcl-2-Associated X Protein - genetics | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Phosphoproteins - genetics | DNA-Binding Proteins - genetics | Imatinib Mesylate | Proto-Oncogene Proteins c-abl - pharmacology | Animals | NF-kappa B - genetics | Colitis, Ulcerative - chemically induced | Adaptor Proteins, Signal Transducing - genetics | Inflammation - genetics | Cell Proliferation - drug effects | Adaptor Proteins, Signal Transducing - metabolism | Tyrosine | Genes | Inflammation | Permeability | Dextran | Cell death | Gastrointestinal diseases | Genetic aspects | Genetic engineering | Colitis | Tumor proteins | Tumors | Cancer | Pediatrics | p53 Protein | Biochemistry | Proteins | Physiology | Tumorigenesis | Inhibition | Damage accumulation | Protein-tyrosine kinase | Deoxyribonucleic acid--DNA | Imatinib | Mortality | Gene expression | Survival | Yes-associated protein | Inflammatory bowel disease | Cell injury | Sodium | Pharmacy | TNF inhibitors | Oxidative stress | Phosphorylation | Inflammatory bowel diseases | Bax protein | Epithelial cells | Gene regulation | DNA damage | Homeostasis | Kinases | Accumulation | Intestine | Rodents | Cell cycle | DNA methylation | Toll-like receptors | Injuries | Pharmaceutical sciences | Cell survival | Dentistry | Immune systems | Medicine | Lymphocytes B | Epigenetics | Tumor suppressor genes | Kidney diseases | Diabetes | Apoptosis | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Journal Article
Journal Article
Journal of Cell Science, ISSN 0021-9533, 07/2010, Volume 123, Issue 14, pp. 2423 - 2433
Tight control of p63 protein levels must be achieved under differentiation or apoptotic conditions. Here, we describe a new regulatory pathway for the Delta... 
MDM2 | p63 | Fbw7 | DNA damage | TRANSCRIPTIONAL ACTIVITY | CYCLIN-E | UBIQUITIN LIGASE | PHOSPHORYLATION | STABILITY | P53 REGULATION | CELL BIOLOGY | TUMOR-SUPPRESSOR | C-JUN | PROMOTES | HUMAN CANCER | F-Box-WD Repeat-Containing Protein 7 | RNA, Small Interfering - genetics | Protein Binding - genetics | Proto-Oncogene Proteins c-mdm2 - genetics | Transcriptional Activation - genetics | Humans | Cell Nucleus - metabolism | Cell Nucleus - radiation effects | Tumor Suppressor Proteins - genetics | Trans-Activators - genetics | Cell Cycle Proteins - genetics | DNA Damage - genetics | Active Transport, Cell Nucleus - genetics | Active Transport, Cell Nucleus - radiation effects | Proto-Oncogene Proteins c-mdm2 - metabolism | Cell Differentiation - radiation effects | Tumor Suppressor Proteins - metabolism | F-Box Proteins - metabolism | Cell Cycle Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Protein Structure, Tertiary - genetics | Mutation - genetics | Ultraviolet Rays - adverse effects | Animals | Cell Differentiation - drug effects | Active Transport, Cell Nucleus - drug effects | Cell Line, Tumor | Trans-Activators - metabolism | Cell Proliferation - drug effects | Mice | Transcription Factors | Cell Nucleus - drug effects | Ubiquitin-Protein Ligases - genetics | F-Box Proteins - genetics | Doxorubicin - pharmacology | Cell Proliferation - radiation effects | Index Medicus
Journal Article