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Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 764 - 17
Checkpoint kinases sense replicative stress to prevent DNA damage. Here we show that the histone deacetylases HDAC1/HDAC2 sustain the phosphorylation of the... 
CANCER-CELLS | RIBONUCLEOTIDE REDUCTASE | CHK1 | TUMOR SUPPRESSION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | GENOME INTEGRITY | DOUBLE-STRAND BREAKS | HISTONE DEACETYLASE INHIBITORS | REPLICATION FORK COLLAPSE | ATR | Phosphorylation | Ataxia Telangiectasia Mutated Proteins - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Tumor Suppressor Protein p53 - genetics | CDC2 Protein Kinase - metabolism | Checkpoint Kinase 2 - metabolism | Checkpoint Kinase 2 - genetics | Protein-Tyrosine Kinases - genetics | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Histone Deacetylase 1 - genetics | Histone Deacetylase 2 - genetics | CDC2 Protein Kinase - genetics | Cell Cycle Proteins - metabolism | Gene Expression Regulation | Protein Phosphatase 2 - genetics | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Checkpoint Kinase 1 - metabolism | Cell Cycle | Protein Phosphatase 2 - metabolism | Histone Deacetylase 2 - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Checkpoint Kinase 1 - genetics | Histone Deacetylase 1 - metabolism | Histone deacetylase | p53 Protein | DNA damage | Serine | Homologous recombination | Homology | Dephosphorylation | Kinases | Phosphatase | Damage prevention | Cell fate | Cell cycle | Inhibition | HDAC2 protein | Null cells | Deoxyribonucleic acid--DNA | Stresses | CHK2 protein | Threonine | Phase transformations | CHK1 protein | Protein-serine/threonine phosphatase | Replication protein A | Protein A | Ablation | Stress | DNA biosynthesis | S phase | Replication | Threonine phosphatase | Phase transition | Tumors | Apoptosis
Journal Article
MOLECULAR AND CELLULAR BIOLOGY, ISSN 0270-7306, 07/2010, Volume 30, Issue 13, pp. 3371 - 3383
ATM-dependent initiation of the radiation-induced G(2)/M checkpoint arrest is well established. Recent results have shown that the majority of DNA... 
STRAND BREAK REPAIR | GENOMIC STABILITY | CHK2 | PHOSPHORYLATION | DNA | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-CYCLE | HOMOLOGOUS RECOMBINATION | RADIOSENSITIVITY | ATAXIA-TELANGIECTASIA | RADIATION | CELL BIOLOGY | Protein Kinases - metabolism | RNA, Small Interfering - genetics | Protein Kinases - genetics | Fibroblasts - physiology | Humans | Intracellular Signaling Peptides and Proteins - metabolism | DNA-Binding Proteins - metabolism | Telomerase - genetics | DNA-Activated Protein Kinase - genetics | DNA-Activated Protein Kinase - metabolism | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Telomerase - metabolism | Signal Transduction - radiation effects | Nuclear Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | DNA-Binding Proteins - physiology | G2 Phase - physiology | G2 Phase - radiation effects | Protein-Serine-Threonine Kinases - physiology | Cells, Cultured | Chromosomal Proteins, Non-Histone | Protein-Serine-Threonine Kinases - genetics | Cell Division - radiation effects | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Mice, Knockout | Cell Division - physiology | Tumor Suppressor Proteins - physiology | Animals | DNA Repair | Endonucleases | Checkpoint Kinase 2 | Checkpoint Kinase 1 | Signal Transduction - physiology | Fibroblasts - cytology | Mice | DNA Damage | Tumor Suppressor p53-Binding Protein 1 | Cell Cycle Proteins - physiology | RNA, Small Interfering - metabolism
Journal Article
Cancer Cell, ISSN 1535-6108, 10/2007, Volume 12, Issue 4, pp. 342 - 354
The tumor suppressor p53 is a transcription factor that responds to cellular stresses by initiating cell cycle arrest or apoptosis. One transcriptional target... 
PROTEINS | CELLCYCLE | TRANSCRIPTIONAL ACTIVATION | CHK2 KINASE | PROTEIN | ONCOLOGY | DNA-DAMAGE RESPONSE | MDM2 | ATM | P53 PATHWAY | CELL-GROWTH | IONIZING-RADIATION | PPM1D | Protein-Serine-Threonine Kinases - deficiency | Fibroblasts - enzymology | Phosphorylation | Proto-Oncogene Proteins c-mdm2 - genetics | Humans | Phosphoprotein Phosphatases - metabolism | Ubiquitin - metabolism | Homeostasis | DNA-Binding Proteins - deficiency | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Transfection | RNA Interference | Time Factors | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ubiquitin Thiolesterase - metabolism | Transcription, Genetic | Signal Transduction - radiation effects | Proto-Oncogene Proteins c-mdm2 - metabolism | Osteosarcoma - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | Osteosarcoma - enzymology | Cell Cycle Proteins - metabolism | Protein Phosphatase 2C | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Serine - metabolism | Mice, Knockout | Animals | Phosphoprotein Phosphatases - genetics | Fibroblasts - radiation effects | Cell Line, Tumor | Phosphoprotein Phosphatases - deficiency | Mice | DNA Damage | Mutation | Osteosarcoma - genetics | Proteasome Endopeptidase Complex - metabolism | Ubiquitin-Specific Peptidase 7 | RNA, Small Interfering - metabolism
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
Journal Article
BMC Cancer, ISSN 1471-2407, 12/2012, Volume 12, Issue 1, pp. 571 - 571
Background: Optimizing the safety and efficacy of standard chemotherapeutic agents such as cisplatin (CDDP) is of clinical relevance. Serum starvation in vitro... 
AMPK | cisplatin therapy | ATM/Chk2/p53 signaling | Serum starvation | short-term food starvation (STS) | PROTEIN-KINASE | DNA-DAMAGE | TUMOR-CELLS | H2AX PHOSPHORYLATION | ONCOGENE | ONCOLOGY | GROWTH | MESOTHELIOMA | ATM ACTIVATION | STRESS | CARCINOMA | Cell Cycle - genetics | Protein Kinases - genetics | Humans | Tumor Suppressor Protein p53 - genetics | Starvation - metabolism | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Cell Line | Tumor Suppressor Proteins - metabolism | HCT116 Cells | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | Cisplatin - pharmacology | DNA-Binding Proteins - genetics | Enzyme Activation - drug effects | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Cell Proliferation - drug effects | Mice | DNA Damage | Cell Cycle - drug effects | Physiological aspects | Genetic aspects | Cellular signal transduction | Research | Cisplatin | Cancer cells | Antimitotic agents | Starvation | Chemotherapy | Lung cancer | Comparative analysis | Antineoplastic agents | Tumor proteins | Cancer
Journal Article
The FEBS Journal, ISSN 1742-464X, 08/2017, Volume 284, Issue 15, pp. 2378 - 2395
The molecular chaperone heat shock protein 90 (Hsp90α) regulates cell proteostasis and mitigates the harmful effects of endogenous and exogenous stressors on... 
H2AX | Hsp90α | 17‐AAG | DNA damage response | DNA double‐strand break | ATM | NBN | ionizing radiation | 17-AAG | DNA double-strand break | CANCER-CELLS | DEPENDENT PHOSPHORYLATION | GENOTOXIC STRESS | MRE11 COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | Hsp90 alpha | HISTONE H2AX | HEAT-SHOCK-PROTEIN | HSP90 INHIBITORS | DAMAGE RESPONSE | CELL-CYCLE | IONIZING-RADIATION | Nijmegen Breakage Syndrome - pathology | Ataxia Telangiectasia Mutated Proteins - metabolism | Checkpoint Kinase 2 - chemistry | Humans | Checkpoint Kinase 1 - chemistry | DNA Breaks, Double-Stranded | Cell Cycle Proteins - chemistry | Checkpoint Kinase 2 - metabolism | Proteasome Endopeptidase Complex - drug effects | Ubiquitination - drug effects | Protein Processing, Post-Translational - drug effects | RNA Interference | Gene Deletion | Ataxia Telangiectasia Mutated Proteins - antagonists & inhibitors | Cell Cycle Proteins - genetics | HSP90 Heat-Shock Proteins - chemistry | Phosphorylation - drug effects | Nuclear Proteins - genetics | DNA Repair - drug effects | Ataxia Telangiectasia Mutated Proteins - chemistry | Nijmegen Breakage Syndrome - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Nuclear Proteins - metabolism | Lactams, Macrocyclic - pharmacology | Nuclear Proteins - chemistry | Nijmegen Breakage Syndrome - genetics | Benzoquinones - pharmacology | Checkpoint Kinase 1 - metabolism | Point Mutation | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Models, Biological | Protein Stability - drug effects | HSP90 Heat-Shock Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Cell Line, Transformed | Protein Multimerization - drug effects | Amino Acid Substitution | Biotechnology | Hsp90 protein | Phosphorylation | DNA damage | Irradiated | Kinases | DNA repair | Degradation | Proteins | Ionizing radiation | MRE11 protein | Fibroblasts | Ataxia | Inhibition | Localization | Repair | Deoxyribonucleic acid--DNA | CHK2 protein | BRCA1 protein | Alpha rays | Lymphoblastoid cell lines | Heat shock proteins | I.R. radiation | Breast cancer | Clients | Damage localization | DNA-dependent protein kinase | Ataxia telangiectasia | Ataxia telangiectasia mutated protein | Control stability | Iridium | Position (location) | Radiation damage | Adenosine triphosphatase | Heat shock
Journal Article
Cancer, ISSN 0008-543X, 05/2017, Volume 123, Issue 10, pp. 1721 - 1730
BACKGROUND As panel testing becomes more common in clinical practice, it is important to understand the prevalence and trends associated with the pathogenic... 
breast cancer type 1 (BRCA1) | panel testing | hereditary breast and ovarian cancer | BRCA2 | triple‐negative breast cancer | triple-negative breast cancer | POPULATION | BRCA2 MUTATIONS | METAANALYSIS | VARIANTS | RISK | PREVALENCE | FAMILY-HISTORY | SUSCEPTIBILITY GENES | COWDEN-SYNDROME | ONCOLOGY | DIFFUSE GASTRIC-CANCER | Genetic Testing | Age Factors | Humans | Middle Aged | Young Adult | Checkpoint Kinase 2 - genetics | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Genes, BRCA2 | Adult | Female | RNA Helicases - genetics | Lynch Syndrome II - genetics | Neoplastic Syndromes, Hereditary - genetics | Genes, BRCA1 | Nuclear Proteins - genetics | Fanconi Anemia Complementation Group N Protein | Hereditary Breast and Ovarian Cancer Syndrome - genetics | DNA-Binding Proteins - genetics | Fanconi Anemia Complementation Group Proteins | Breast Neoplasms - genetics | Triple Negative Breast Neoplasms - genetics | Aged | Ataxia Telangiectasia Mutated Proteins - genetics | Ubiquitin-Protein Ligases - genetics | Women | Breast cancer | Genetic aspects | Diagnosis | Research | Health aspects | Oncogenes | BRCA2 protein | CHK2 protein | Threonine | BRCA1 protein | Genes | Health risks | Protein C | Genetic screening | DNA helicase | Men | Breast | Ataxia | Ataxia telangiectasia mutated protein | Protein-serine/threonine kinase | Mutation | Health risk assessment | Age | Cancer | Index Medicus | Abridged Index Medicus
Journal Article
Cancer, ISSN 0008-543X, 10/2017, Volume 123, Issue 20, pp. 3925 - 3932
BACKGROUND Prostate cancer has a significant heritable component, and rare deleterious germline variants in certain genes can increase the risk of the disease.... 
prostate cancer | germline variants | multiple primary malignant neoplasms | genetic testing | gene panel | GENOMICS | ONCOLOGY | COLORECTAL-CANCER | DNA | HOXB13 G84E MUTATION | RISK | LYNCH SYNDROME | Humans | Middle Aged | Male | Mutation, Missense | Checkpoint Kinase 2 - genetics | Prostatic Neoplasms - genetics | DNA Mutational Analysis | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Germ-Line Mutation | Adult | RNA Helicases - genetics | Neoplastic Syndromes, Hereditary - genetics | Neoplasms, Second Primary - genetics | Nuclear Proteins - genetics | Fanconi Anemia Complementation Group N Protein | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Genetic Predisposition to Disease | Neoplastic Syndromes, Hereditary - diagnosis | DNA-Binding Proteins - genetics | Fanconi Anemia Complementation Group Proteins | Sequence Analysis, DNA | Homeodomain Proteins - genetics | MutL Protein Homolog 1 - genetics | Age of Onset | Aged | Ataxia Telangiectasia Mutated Proteins - genetics | BRCA2 Protein - genetics | Care and treatment | Genetic aspects | Research | Gene mutations | Genetic variation | Prostate cancer | Fibroblast growth factor | Genes | DNA damage | Medical services | Homology | Malignancy | Criteria | DNA repair | Genetic screening | Homeobox | DNA helicase | Proteins | Ataxia | Genetics | Deoxyribonucleic acid--DNA | Fibroblast growth factor receptor 3 | BRCA2 protein | CHK2 protein | Nucleotide sequence | BRCA1 protein | MLH1 protein | Health risks | Protein C | Breast cancer | Medical screening | Patients | Medical prognosis | Men | Ataxia telangiectasia mutated protein | Mutation | Prostate | Cancer | Fibroblast growth factor receptors
Journal Article
Nature Chemical Biology, ISSN 1552-4450, 2011, Volume 7, Issue 7, pp. 428 - 430
Journal Article
Journal Article
PLoS pathogens, ISSN 1553-7366, 2009, Volume 5, Issue 10, pp. e1000605 - e1000605
Human papillomaviruses (HPV) are the causative agents of cervical cancers. The infectious HPV life cycle is closely linked to the differentiation state of the... 
LIFE-CYCLE | DEPENDENT PHOSPHORYLATION | MRE11 COMPLEX | PROTEIN-KINASE | DOUBLE-STRAND BREAKS | MICROBIOLOGY | HISTONE H2AX | EPITHELIAL DIFFERENTIATION | S-PHASE CHECKPOINT | REPAIR PROTEINS | VIROLOGY | IONIZING-RADIATION | PARASITOLOGY | Immunohistochemistry | Blotting, Southern | Genome, Viral | Tumor Suppressor Proteins - metabolism | Immunoprecipitation | Keratinocytes - virology | Humans | Cell Cycle Proteins - metabolism | In Situ Hybridization, Fluorescence | Keratinocytes - cytology | Ataxia Telangiectasia Mutated Proteins | Blotting, Western | Papillomaviridae - genetics | DNA-Binding Proteins - metabolism | Papillomaviridae - pathogenicity | Papillomavirus E7 Proteins - metabolism | Papillomavirus Infections - metabolism | Fluorescent Antibody Technique | Checkpoint Kinase 2 | Signal Transduction - physiology | Cell Differentiation - physiology | Virus Replication - physiology | Protein-Serine-Threonine Kinases - metabolism | Complications and side effects | Gene amplification | Care and treatment | DNA damage | Physiological aspects | Genetic aspects | Research | Papillomavirus infections | Protein kinases | Phosphorylation | Protein kinase C | Epithelial cells | Mucosa | Genomes | Drug development | E7 protein | Caspase-3 | Anogenital | Life cycle | Signal transduction | Virions | Cell cycle | Antiviral agents | Pathogens | CHK2 protein | BRCA1 protein | Keratinocytes | Gene expression | DNA biosynthesis | Infection | Replication | Differentiation | Cervical cancer | Cancer | Proteins | Human papillomavirus | Microbiology | Kinases | DNA repair
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 06/2012, Volume 287, Issue 23, pp. 18937 - 18952
Journal Article