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by McRae, Jeremy F and Clayton, Stephen and Fitzgerald, Tomas W and Kaplanis, Joanna and Prigmore, Elena and Rajan, Diana and Sifrim, Alejandro and Aitken, Stuart and Akawi, Nadia and Alvi, Mohsan and Ambridge, Kirsty and Barrett, Daniel M and Bayzetinova, Tanya and Jones, Philip and Jones, Wendy D and King, Daniel and Krishnappa, Netravathi and Mason, Laura E and Singh, Tarjinder and Tivey, Adrian R and Ahmed, Munaza and Anjum, Uruj and Archer, Hayley and Armstrong, Ruth and Awada, Jana and Balasubramanian, Meena and Banka, Siddharth and Baralle, Diana and Barnicoat, Angela and Batstone, Paul and Baty, David and Bennett, Chris and Berg, Jonathan and Bernhard, Birgitta and Bevan, A. Paul and Bitner-Glindzicz, Maria and Blair, Edward and Blyth, Moira and Bohanna, David and Bourdon, Louise and Bourn, David and Bradley, Lisa and Brady, Angela and Brent, Simon and Brewer, Carole and Brunstrom, Kate and Bunyan, David J and Burn, John and Canham, Natalie and Castle, Bruce and Chandler, Kate and Chatzimichali, Elena and Cilliers, Deirdre and Clarke, Angus and Clasper, Susan and Clayton-Smith, Jill and Clowes, Virginia and Coates, Andrea and Cole, Trevor and Colgiu, Irina and Collins, Amanda and Collinson, Morag N and Connell, Fiona and Cooper, Nicola and Cox, Helen and Cresswell, Lara and Cross, Gareth and Crow, Yanick and D'Alessandro, Mariella and Dabir, Tabib and Davidson, Rosemarie and Davies, Sally and De Vries, Dylan and Dean, John and Deshpande, Charu and Devlin, Gemma and Dixit, Abhijit and Dobbie, Angus and Donaldson, Alan and Donnai, Dian and Donnelly, Deirdre and Donnelly, Carina and Douglas, Angela and Douzgou, Sofia and Duncan, Alexis and Eason, Jacqueline and Ellard, Sian and Ellis, Ian and Elmslie, Frances and Evans, Karenza and Everest, Sarah and Fendick, Tina and Fisher, Richard and Flinter, Frances and Foulds, Nicola and Fry, Andrew and Fryer, Alan and Gardiner, Carol and Gaunt, Lorraine and Ghali, Neeti and ... and Deciphering Developmental Disorders Study
Nature (London), ISSN 1476-4687, 01/2017, Volume 542, Issue 7642, pp. 433 - 438
The genomes of individuals with severe, undiagnosed developmental disorders are enriched in damaging de novo mutations (DNMs) in developmentally important... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Prevalence | Humans | Middle Aged | Parents | Male | Mi-2 Nucleosome Remodeling and Deacetylase Complex - genetics | Developmental Disabilities - genetics | Casein Kinase II - genetics | Autoantigens - genetics | Young Adult | ras GTPase-Activating Proteins - genetics | Adult | Female | Child | CDC2 Protein Kinase - genetics | Histone-Lysine N-Methyltransferase - genetics | Repressor Proteins - genetics | Sex Characteristics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Mutation - genetics | Nerve Tissue Proteins - genetics | Sequence Analysis, DNA | Homeodomain Proteins - genetics | DEAD-box RNA Helicases - genetics | Exome - genetics | Phenotype | Myeloid-Lymphoid Leukemia Protein - genetics | Adolescent | Heredity - genetics | Protein Phosphatase 2C - genetics | Cohort Studies | Child development deviations | Genetic aspects | Genetic disorders | Developmental disabilities | Distribution | Genes | Families & family life | Births | Genomes | Mutation | Causality | Estimates | Age | Index Medicus | TRIO | MYT1L | EHMT1 | HNRNPU | SUV420H1 | COL4A3BP | SYNGAP1 | PPP2R1A | POGZ | EP300 | KCNH1 | SCN1A | MEF2C | CDKL5 | CSNK2A1 | DYRK1A | CASK | ALG13 | FOXP1 | KAT6B | TBL1XR1 | KAT6A | SCN8A | KCNQ2 | EEF1A2 | KCNQ3 | ADNP | PhenIcons | SET | KMT2A | ANKRD11 | STXBP1 | FOXG1 | ZC4H2 | ITPR1 | De novo mutation | Seizures | ZBTB18 | CREBBP | SMAD4 | PDHA1 | IQSEC2 | AUTS2 | BCL11A | BRAF | SMARCA2 | GRIN2B | MED13L | GNAO1 | CNOT3 | TCF4 | SCN2A | CDK13 | GABRB3 | SETD5 | KDM5B | Developmental Disease | DDX3X | CHD8 | PTEN | CHD4 | TCF20 | CTCF | CHD2 | WDR45 | SLC6A1 | MECP2 | CHAMP1 | KIF1A | Average Faces | MSL3 | PPP2R5D | SMC1A | ARID1B | DNM1 | CNKSR2 | PACS1 | WAC | ZMYND11 | AHDC1 | NFIX | SATB2 | HDAC8 | PPM1D | GNAI1 | PURA | PUF60 | NSD1 | Intellectual Disability | SLC35A2 | DYNC1H1 | NAA10 | USP9X | PTPN11 | GATAD2B | ASXL1 | KANSL1 | ASXL3 | CTNNB1 | QRICH1
Journal Article
Nature communications, ISSN 2041-1723, 02/2018, 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... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | 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 | Phase transitions | Cell fate | Cell cycle | Inhibition | HDAC2 protein | Null cells | Deoxyribonucleic acid--DNA | Stresses | CHK2 protein | Threonine | CHK1 protein | Protein-serine/threonine phosphatase | Replication protein A | Protein A | Ablation | Stress | DNA biosynthesis | S phase | Replication | Threonine phosphatase | Tumors | Apoptosis | Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, pp. e0123819 - e0123819
Objective In this study, the anticancer mechanisms of MT-4 were examined in A2780 and multidrug-resistant NCI-ADR/res human ovarian cancer cell lines. Methods... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Aurora Kinase B - metabolism | Cyclin-Dependent Kinases - metabolism | Tubulin Modulators - pharmacology | Humans | Caspase 3 - metabolism | Ovarian Neoplasms - pathology | HSP27 Heat-Shock Proteins - genetics | Ovarian Neoplasms - genetics | Cyclin B - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | Caspase 3 - genetics | Ovarian Neoplasms - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Protein-Serine-Threonine Kinases - metabolism | Carcinoma - drug therapy | Signal Transduction | Cell Cycle Proteins - metabolism | Imidazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Benzyl Compounds - pharmacology | Cell Line, Tumor | HSP27 Heat-Shock Proteins - metabolism | Carcinoma - genetics | Mice | Histones - metabolism | CDC2 Protein Kinase | Gene Expression Regulation, Neoplastic | Tubulin - genetics | Tubulin - metabolism | Cell Cycle Proteins - genetics | Female | Antineoplastic Agents - pharmacology | HSP27 Heat-Shock Proteins - antagonists & inhibitors | Carcinoma - pathology | Cyclin-Dependent Kinases - genetics | Ovarian Neoplasms - drug therapy | Proto-Oncogene Proteins - metabolism | Aurora Kinase B - genetics | Protein-Serine-Threonine Kinases - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Proto-Oncogene Proteins - genetics | Xenograft Model Antitumor Assays | Animals | Histones - genetics | Cyclin B - metabolism | Cell Proliferation - drug effects | Pyridines - pharmacology | Carcinoma - metabolism | Drug Resistance, Neoplasm - drug effects | Chemotherapy | Growth | Analysis | Polymerization | Heat shock proteins | Tubulins | Ovarian cancer | Cancer | Apoptosis | Cytochrome | Cdc2 protein | Ovarian carcinoma | Polo-like kinase 1 | Immunoblotting | Aurora kinase | Metastasis | Drug resistance | Kinases | Assaying | Caspase-3 | Cancer therapies | Angiogenesis | Tubulin | Cyclin B | Penicillin | Xenografts | Cell cycle | Polo-like kinase | Inhibition | P-Glycoprotein | Immunoglobulins | Poly(ADP-ribose) polymerase | Caspase | MAP kinase | Glycoproteins | Fluorides | Tumor cell lines | Substrates | Plasmids | Hsp27 protein | Pharmacy | Phenols | Histone H3 | Heat shock | Tumors | Index Medicus
Journal Article
Cell reports (Cambridge), ISSN 2211-1247, 12/2015, Volume 13, Issue 11, pp. 2425 - 2439
... networks commonly altered in GBM and GSCs (e.g., oncogenic drivers). In vitro and in vivo validation of GSC-specific targets revealed several strong hits, including the wee1-like kinase, PKMYT1/Myt1... 
WEE1 | CRISPR-Cas9 | Glioblastoma | cancer therapeutics | functional genomics | PKMYT1 | gene editing | Myt1 | Cancer therapeutics | Gene editing | Functional genomics | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Neoplastic Stem Cells - cytology | Phosphorylation | Mitosis | Protein-Tyrosine Kinases - metabolism | Humans | Microscopy, Video | Time-Lapse Imaging | Tumor Suppressor Protein p53 - genetics | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - genetics | Neoplastic Stem Cells - metabolism | RNA Interference | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Glioblastoma - metabolism | Membrane Proteins - metabolism | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Protein-Serine-Threonine Kinases - metabolism | Pyrazoles - pharmacology | Cell Survival - drug effects | ErbB Receptors - metabolism | Gene Library | CDC2 Protein Kinase - antagonists & inhibitors | Membrane Proteins - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Pyrimidinones | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Pyrimidines - pharmacology | CRISPR-Cas Systems - genetics | Membrane Proteins - antagonists & inhibitors | Glioblastoma - pathology | Nuclear Proteins - antagonists & inhibitors | Cyclin B - metabolism | Genome, Human | Protein-Tyrosine Kinases - antagonists & inhibitors | Index Medicus
Journal Article
Journal Article
Biology of Reproduction, ISSN 0006-3363, 02/2008, Volume 78, Issue 2, pp. 218 - 233
Maturation of immature bovine oocytes requires cytoplasmic polyadenylation and synthesis of a number of proteins involved in meiotic progression and metaphase-II arrest... 
Gamete biology | Aurora kinases | Bovine | CPEB | Meiosis | Oocyte development | Kinases | Oocyte | Life Sciences & Biomedicine | Reproductive Biology | Science & Technology | Protein-Serine-Threonine Kinases - analysis | Nitriles - pharmacology | mRNA Cleavage and Polyadenylation Factors - metabolism | Cytoplasm - metabolism | RNA, Messenger - metabolism | Cyclin B1 | Embryo, Mammalian - metabolism | Aurora Kinase A | CDC2 Protein Kinase - metabolism | Proto-Oncogene Proteins c-mos - genetics | Aurora Kinase B | Aurora Kinase C | Meiosis - drug effects | Cyclin B - genetics | Cattle | Female | Proto-Oncogene Proteins c-mos - metabolism | mRNA Cleavage and Polyadenylation Factors - genetics | Protein-Serine-Threonine Kinases - metabolism | Cytoplasm - chemistry | mRNA Cleavage and Polyadenylation Factors - analysis | Butadienes - pharmacology | CDC2 Protein Kinase - genetics | Oocytes - growth & development | Fertilization | Oocytes - metabolism | Purines - pharmacology | Metformin - pharmacology | Oocytes - chemistry | Protein-Serine-Threonine Kinases - genetics | Aurora Kinases | Piperazines - pharmacology | Proto-Oncogene Proteins c-mos - analysis | Cyclin B - analysis | Animals | Polyadenylation | CDC2 Protein Kinase - analysis | Cyclin B - metabolism | Protein Kinase Inhibitors - pharmacology | Index Medicus | CDC2 Protein Kinase | Piperazines | Embryo, Mammalian | Protein-Serine-Threonine Kinases | Proto-Oncogene Proteins c-mos | Butadienes | Cellular Biology | Oocytes | Life Sciences | Purines | Protein Kinase Inhibitors | Cyclin B | Nitriles | Metformin | RNA, Messenger | mRNA Cleavage and Polyadenylation Factors | Cytoplasm
Journal Article
Current genetics, ISSN 0172-8083, 5/2017, Volume 63, Issue 2, pp. 275 - 280
.... The S phase checkpoint kinase Mec1/ATR inhibits mitotic Cyclin Dependent Kinase activity through effector kinases Swe1/Wee1 and Rad53/Chk2... 
Biochemistry, general | S Phase checkpoint | Microbiology | DNA damage response (DDR) | Chromosome segregation | Cell Biology | Genomic instability | Life Sciences | Spindle assembly checkpoint (SAC) | Microbial Genetics and Genomics | Proteomics | Cyclin Dependent Kinase (Cdk1) | Plant Sciences | Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | DNA, Fungal - genetics | Saccharomyces cerevisiae - genetics | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Securin - metabolism | S Phase Cell Cycle Checkpoints - genetics | CDC2 Protein Kinase - metabolism | Checkpoint Kinase 2 - metabolism | Saccharomyces cerevisiae - metabolism | Checkpoint Kinase 2 - genetics | Spindle Apparatus - genetics | Securin - genetics | Cell Cycle Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | CDC2 Protein Kinase - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Saccharomyces cerevisiae Proteins - genetics | Anaphase - genetics | DNA, Fungal - metabolism | Saccharomyces cerevisiae Proteins - metabolism | Models, Genetic | DNA Damage | Mutation | Chromosome Segregation - genetics | Chromosome replication | Medical colleges | DNA damage | DNA | Molecular biology | Chromosomes | DNA repair | Phosphotransferases | Index Medicus | Original
Journal Article