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Molecular Cancer Therapeutics, ISSN 1535-7163, 01/2017, Volume 16, Issue 1, pp. 25 - 34
AZD6738 is an orally active ATR inhibitor (ATRi) currently in phase I clinical trials. We found in vitro growth inhibitory activity of this ATRi in a panel of... 
CANCER-CELLS | ONCOLOGY | CONSEQUENCES | SENSITIVITY | TUMOR-CELLS | CHECKPOINT | IDENTIFICATION | CHROMOTHRIPSIS | STRESS | DEPENDENT MANNER | RADIATION | Homologous Recombination - drug effects | Tumor Burden - radiation effects | Humans | Tumor Suppressor Protein p53 - genetics | G2 Phase Cell Cycle Checkpoints - radiation effects | G2 Phase Cell Cycle Checkpoints - drug effects | Micronuclei, Chromosome-Defective - drug effects | Inhibitory Concentration 50 | Micronuclei, Chromosome-Defective - radiation effects | Disease Models, Animal | Radiation, Ionizing | DNA Damage - drug effects | Sulfoxides - pharmacology | Homologous Recombination - radiation effects | Radiation-Sensitizing Agents - pharmacology | Tumor Suppressor Protein p53 - metabolism | Pyrimidines - pharmacology | Radiation Tolerance - drug effects | Xenograft Model Antitumor Assays | Animals | Tumor Burden - drug effects | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | DNA Damage - radiation effects | Biotechnology | Mitosis | p53 Protein | DNA damage | Homologous recombination | Cytology | Radiation | Clinical trials | Fluorescence | Homology | Nuclei | Ubiquitination | Radiosensitization | Inhibition | Deoxyribonucleic acid--DNA | BRCA2 protein | Medical research | Radiation effects | CHK1 protein | Breast cancer | Tumor cell lines | Inhibitors | Micronuclei | Cell lines | Nuclei (cytology) | Three dimensional models | Radiation damage | Cancer
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2010, Volume 5, Issue 8, p. e12112
textabstractApproximately half of cancer-affected patients receive radiotherapy (RT). The doses delivered have been determined upon empirical experience based... 
SISTER-CHROMATID COHESION | STEM-CELLS | BIOLOGY | VERTEBRATE CELLS | DOUBLE-STRAND BREAKS | SMALL-INTESTINE | HOMOLOGOUS RECOMBINATION | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | SACCHAROMYCES-CEREVISIAE | RADIATION-INDUCED APOPTOSIS | Sister Chromatid Exchange - genetics | Whole-Body Irradiation | Epithelial Cells - metabolism | Embryo, Mammalian | Genetic Loci - genetics | DNA Repair - radiation effects | Gastrointestinal Tract - radiation effects | DNA Repair - genetics | Stem Cells - metabolism | Gene Deletion | Nuclear Proteins - deficiency | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Fibroblasts - metabolism | Cell Line | Chromosome Aberrations - radiation effects | Epithelial Cells - radiation effects | Mitosis - radiation effects | Bone Marrow Cells - cytology | Stem Cells - radiation effects | Radiation Tolerance - genetics | Phosphoproteins - genetics | Chromosomal Proteins, Non-Histone - deficiency | Gastrointestinal Tract - metabolism | Chromosomal Proteins, Non-Histone - genetics | Mitomycin - pharmacology | Sister Chromatid Exchange - drug effects | Animals | Fibroblasts - radiation effects | Intestine, Small - cytology | Phosphoproteins - deficiency | Sister Chromatid Exchange - radiation effects | Gastrointestinal Tract - cytology | Mice | DNA Damage | DNA damage | Gastrointestinal system | DNA | Stem cells | Radiation | Radiotherapy | DNA repair | Radiosensitivity | Homologous recombination | Inactivation | Cancer therapies | Eukaryotes | Ionizing radiation | Animal tissues | Bone marrow | Genetics | Growth factors | Chromosomes | Deoxyribonucleic acid--DNA | Mammals | Patients | Embryos | Irradiation | Cohesin | Radiation damage | Cohesion | Senescence | Yeast | Laboratories | Toxicity | Genes | Homology | Oncology | Biology | Gene deletion | Gene targeting | Clonal deletion | Deletion | Gene dosage | Cell survival | Deactivation | Hypersensitivity | Organs | I.R. radiation | Gastrointestinal tract | Radiation therapy | Mutants | Haploinsufficiency | Regeneration | Cancer | Apoptosis | Deoxyribonucleic acid
Journal Article
Plant Physiology, ISSN 0032-0889, 2/2013, Volume 161, Issue 2, pp. 1034 - 1048
The regulation of carbon metabolism in the diatom Phaeodactylum tricornutum at the cell, metabolite, and gene expression levels in exponential fed-batch... 
Enzymes | Scotophase | Photophase | Genes | SYSTEMES AND SYNTHETIC BIOLOGY | Lipids | Gene expression regulation | Biosynthesis | Diatoms | Gene expression | Fatty acids | FATTY-ACID COMPOSITION | MARINE DIATOM | GLYCOLYTIC PATHWAY | MICROALGAE | MITOTIC CHROMOSOME | DARK CYCLE | CELL-CYCLE | NUTRIENT LIMITATION | CARBOHYDRATE-METABOLISM | PHYTOPLANKTON | PLANT SCIENCES | Oligonucleotide Array Sequence Analysis | Diatoms - genetics | Carbohydrate Metabolism - genetics | Gene Expression Profiling | Phylogeny | Pyruvate Dehydrogenase Complex - genetics | Mitosis - genetics | Acclimatization - radiation effects | Diatoms - metabolism | Glycolysis - genetics | Diatoms - radiation effects | Mitochondria - genetics | Membrane Transport Proteins - genetics | Mitochondria - radiation effects | Plastids - genetics | Lipid Metabolism - genetics | Plastids - metabolism | Carbon - metabolism | Mitosis - radiation effects | Carbon Cycle - genetics | Lipid Metabolism - radiation effects | Mitochondria - metabolism | Photoperiod | Pyruvate Dehydrogenase Complex - classification | Carbohydrate Metabolism - radiation effects | Gluconeogenesis - genetics | Gluconeogenesis - radiation effects | Membrane Transport Proteins - classification | Glycolysis - radiation effects | Gene Expression Regulation - radiation effects | Acclimatization - genetics | Plastids - radiation effects | Circadian rhythms | Physiological aspects | Acclimatization | Genetic aspects | Genetic regulation | Carbon
Journal Article
Cancer Cell, ISSN 1535-6108, 2007, Volume 11, Issue 2, pp. 175 - 189
In response to DNA damage, eukaryotic cells activate ATM-Chk2 and/or ATR-Chk1 to arrest the cell cycle and initiate DNA repair. We show that, in the absence of... 
SIGNALING | CANCER-CELLS | ONCOLOGY | 7-HYDROXYSTAUROSPORINE UCN-01 | MITOTIC CATASTROPHE | SECKEL-SYNDROME | MAPKAP KINASE-2 | NUCLEAR EXPORT | INDUCED CYTOTOXICITY | 14-3-3 PROTEIN-BINDING | RADIOSENSITIZING AGENT | PHOSPHORYLATION SITES | Protein Kinases - genetics | Antibiotics, Antineoplastic - pharmacology | Humans | DNA Repair - radiation effects | Staurosporine - analogs & derivatives | Bone Neoplasms - pathology | G2 Phase - drug effects | Bone Neoplasms - metabolism | DNA-Binding Proteins - metabolism | Neoplasms, Experimental - pathology | Tumor Suppressor Protein p53 - physiology | Ultraviolet Rays | Antineoplastic Agents - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | cdc25 Phosphatases - metabolism | Osteosarcoma - metabolism | Protein-Serine-Threonine Kinases - metabolism | DNA Damage - drug effects | DNA Repair - drug effects | Tumor Suppressor Proteins - metabolism | Mitosis - radiation effects | G2 Phase - radiation effects | Signal Transduction | Cell Survival | Cell Cycle Proteins - metabolism | Cells, Cultured | Cell Division - radiation effects | Intracellular Signaling Peptides and Proteins | Protein Kinase C - antagonists & inhibitors | Ataxia Telangiectasia Mutated Proteins | Cisplatin - pharmacology | Cell Division - drug effects | Mice, Knockout | Phosphorylation - radiation effects | S Phase - radiation effects | Animals | Mitosis - drug effects | Mice, Nude | Protein Kinases - physiology | Mice | S Phase - drug effects | Neoplasms, Experimental - metabolism | DNA Damage - radiation effects | Doxorubicin - pharmacology | Osteosarcoma - pathology | Staurosporine - pharmacology | DNA
Journal Article
Journal Article
The EMBO Journal, ISSN 0261-4189, 12/2006, Volume 25, Issue 24, pp. 5775 - 5782
The phosphatidyl inositol 3‐kinase‐like kinases (PIKKs), ataxia‐telangiectasia mutated (ATM) and ATM‐ and Rad3‐related (ATR) regulate parallel damage response... 
ataxia telangiectasia‐mutated protein | PIKKs | phosphorylation | DNA damage responses | Phosphorylation | Ataxia telangiectasia-mutated protein | RECRUITMENT | BIOCHEMISTRY & MOLECULAR BIOLOGY | ataxia telangiectasia-mutated protein | DNA-DAMAGE | COMPLEXES | PROTEIN-KINASES | CELL BIOLOGY | CHK1 | SECKEL-SYNDROME | CHECKPOINT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | BINDING | Protein Kinases - metabolism | Hydroxyurea - pharmacology | Protein-Serine-Threonine Kinases - deficiency | DNA Replication - drug effects | Humans | G2 Phase - drug effects | DNA-Binding Proteins - metabolism | Ultraviolet Rays | DNA Replication - radiation effects | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Tumor Suppressor Proteins - metabolism | Mitosis - radiation effects | G2 Phase - radiation effects | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | Enzyme Activation - drug effects | Fibroblasts - pathology | Phosphoserine - metabolism | Enzyme Activation - radiation effects | Histones - deficiency | Phosphorylation - radiation effects | Animals | Mitosis - drug effects | Fibroblasts - radiation effects | Models, Biological | Fibroblasts - drug effects | Phosphoproteins - deficiency | Checkpoint Kinase 2 | Checkpoint Kinase 1 | Fibroblasts - cytology | Mice | Ions | Ultraviolet radiation | Molecular biology | Kinases | DNA damage
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 11/2017, Volume 24, Issue 11, pp. 1853 - 1860
Ionizing radiation (IR) is one of the most widely used treatments for cancer. However, acute damage to the gastrointestinal tract or gastrointestinal acute... 
GASTROINTESTINAL-SYNDROME | STRAND BREAK REPAIR | P53-DEFICIENT MICE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | MITOTIC CATASTROPHE | DEPENDENT PROTEIN-KINASE | SMALL-INTESTINE | CHECKPOINT ACTIVATION | IONIZING-RADIATION | REPLICATION STRESS | CELL BIOLOGY | Stem Cell Niche - radiation effects | Receptors, G-Protein-Coupled - metabolism | Apoptosis - radiation effects | Mitosis | Gastrointestinal Tract - radiation effects | Stem Cells - metabolism | Gastrointestinal Tract - pathology | DNA-Binding Proteins - metabolism | Radiation Tolerance - radiation effects | Acute Radiation Syndrome - pathology | DNA-Activated Protein Kinase - metabolism | Acute Radiation Syndrome - metabolism | Inhibitor of Apoptosis Proteins - metabolism | Repressor Proteins - metabolism | Radiation, Ionizing | Paneth Cells - metabolism | Mice, Inbred C57BL | Stem Cells - radiation effects | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Survivin | Mitotic Index | Phenotype | Phosphorylation - radiation effects | Animals | Staining and Labeling | Stem Cells - pathology | DNA Damage | Histones - metabolism | Cell Proliferation - radiation effects | Cell proliferation | Animal models | Radiosensitivity | Epithelial cells | p53 Protein | DNA damage | DNA repair | Ionizing radiation | Intestine | Rodents | Cell cycle | Repair | Deoxyribonucleic acid--DNA | I.R. radiation | Gastrointestinal tract | Paneth cells | DNA-dependent protein kinase | Cell death | Stem cells | Tumor suppressor genes | Sensitivity enhancement | Mutation | Radiation damage | Tumors | Apoptosis | Cancer | Original Paper
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2014, Volume 9, Issue 4, p. e94967
Knowledge of the mechanisms involved in the radiation response is critical for developing interventions to mitigate radiation-induced injury to normal tissues.... 
TOTAL-BODY IRRADIATION | GASTROINTESTINAL-SYNDROME | BONE-MARROW INJURY | STEM-CELLS | BINDING-PROTEIN-DELTA | PLASMA CITRULLINE | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | SELECTIVELY PROTECTS | CELLULAR-RESPONSE | Myeloid Cells - cytology | Apoptosis - radiation effects | Intestines - radiation effects | Radiation Tolerance | Whole-Body Irradiation - adverse effects | Blood Cells - cytology | CCAAT-Enhancer-Binding Protein-delta - deficiency | CCAAT-Enhancer-Binding Protein-delta - metabolism | Leukocytes, Mononuclear - radiation effects | Citrulline - blood | Hematopoietic Stem Cells - radiation effects | Mitosis - radiation effects | Bone Marrow Cells - cytology | Intestines - injuries | Animals | Blood Cells - radiation effects | Hematopoietic Stem Cells - cytology | Myeloid Cells - radiation effects | Radiation Injuries - blood | Gene Expression Regulation - radiation effects | Leukocytes, Mononuclear - cytology | Radiation Injuries - pathology | Mice | DNA Damage | Histones - metabolism | Radiation Injuries - metabolism | Intestines - cytology | Osteoprogenitor cells | Oxidative stress | Post-irradiation | Transcription factors | Genes | DNA damage | Erythrocytes | Stem cell transplantation | Leukocytes (mononuclear) | Lethality | CCAAT/enhancer-binding protein | Genomic instability | Proteins | Nuclear accidents & safety | Ionizing radiation | Allografts | Immunology | Intestine | Rodents | Animal tissues | Bone marrow | Radiation injuries | Injuries | Pharmaceutical sciences | Deoxyribonucleic acid--DNA | Medical research | Radiation effects | Myeloid cells | Stability | Blood cells | Leukocytes (neutrophilic) | Exposure | Radiation therapy | Citrulline | White blood cells | Stromal cells | Crypts | Stem cells | Cells (biology) | Irradiation | Bone | Laboratory animals | Platelets | Radiation damage | Apoptosis | Cancer | Deoxyribonucleic acid | DNA
Journal Article