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Molecular Biology of the Cell, ISSN 1059-1524, 04/2011, Volume 22, Issue 8, pp. 1191 - 1206
Mitosis requires precise coordination of multiple global reorganizations of the nucleus and cytoplasm. Cyclin-dependent kinase 1 (Cdk1) is the primary upstream... 
ANAPHASE-PROMOTING COMPLEX | XENOPUS EGG EXTRACTS | PROTEIN PHOSPHATASES | CYCLE-DEPENDENT PHOSPHORYLATION | UBIQUITIN LIGASE | M-PHASE | CHROMOSOME ALIGNMENT | CELL-CYCLE | TUMOR-CELLS | SPINDLE-ASSEMBLY CHECKPOINT | CELL BIOLOGY | Cyclin-Dependent Kinases - metabolism | Gene Expression - drug effects | Xenopus Proteins - genetics | Mitosis | Protein-Tyrosine Kinases - metabolism | Humans | Phosphoprotein Phosphatases - metabolism | G2 Phase - drug effects | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - genetics | Cyclin B - genetics | cdc25 Phosphatases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Prometaphase - drug effects | Female | Cyclin-Dependent Kinases - antagonists & inhibitors | Phosphorylation - drug effects | cdc25 Phosphatases - metabolism | Cyclin-Dependent Kinases - genetics | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | CDC2 Protein Kinase - genetics | Protein Phosphatase 2 - antagonists & inhibitors | CDC2 Protein Kinase - antagonists & inhibitors | Xenopus laevis | Cell Cycle Proteins - metabolism | Protein Phosphatase 2 - genetics | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | Phosphoprotein Phosphatases - antagonists & inhibitors | cdc25 Phosphatases - genetics | Xenopus Proteins - antagonists & inhibitors | Membrane Proteins | Animals | Phosphoprotein Phosphatases - genetics | Nuclear Proteins - antagonists & inhibitors | Protein Phosphatase 2 - metabolism | Cyclin B - metabolism | Feedback, Physiological - drug effects | Xenopus Proteins - metabolism | Protein Kinase Inhibitors - pharmacology | S Phase - drug effects | HeLa Cells | Protein-Tyrosine Kinases - antagonists & inhibitors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 06/2009, Volume 459, Issue 7248, pp. 852 - 856
Cells normally grow to a certain size before they enter mitosis and divide. Entry into mitosis depends on the activity of Cdk1, which is inhibited by the Wee1... 
FISSION YEAST | WEE1 | PHOSPHORYLATION | NIM1/CDR1 MITOTIC INDUCER | PROTEIN-KINASE | NEGATIVE REGULATION | MULTIDISCIPLINARY SCIENCES | GROWTH | DIVISION PLANE | DUAL-SPECIFICITY KINASE | SCHIZOSACCHAROMYCES-POMBE | Protein Kinases - metabolism | Cell Polarity | Phosphorylation | Mitosis | Protein-Tyrosine Kinases - metabolism | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Protein Transport | Cell Cycle Proteins - antagonists & inhibitors | Schizosaccharomyces - metabolism | Nuclear Proteins - antagonists & inhibitors | ras-GRF1 - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Schizosaccharomyces pombe Proteins - metabolism | Cell Cycle - physiology | G2 Phase | Protein-Serine-Threonine Kinases - metabolism | Schizosaccharomyces - cytology | Fungal Proteins - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Schizosaccharomyces pombe Proteins - antagonists & inhibitors | Arctic research | Cell cycle | Physiological aspects | Cell physiology | Genetic aspects | Research | Protein kinases | Proteins | Cell growth | Kinases | Molecular biology | Monitoring systems | Index Medicus | ras-GRF1 | Protein-Serine-Threonine Kinases | Schizosaccharomyces pombe Proteins | Fungal Proteins | Cellular Biology | Nuclear Proteins | Life Sciences | Cell Cycle | Protein Kinases | Protein-Tyrosine Kinases | Cell Cycle Proteins | Schizosaccharomyces
Journal Article
Science, ISSN 0036-8075, 2/2013, Volume 339, Issue 6120, pp. 711 - 715
Journal Article
Cell, ISSN 0092-8674, 03/2018, Volume 173, Issue 1, pp. 104 - 116.e12
Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a... 
heart failure | cyclin | proliferation | cell cycle | regeneration | cytokinesis | cardiomyocyte | cell division | CDK | heart | HYPERTROPHY | INFARCTION | EXPRESSION ANALYSIS | AMPLIFICATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MICE | ZEBRAFISH HEART REGENERATION | FAILURE | CANCER | FIBROBLASTS | PROGRAM | CELL BIOLOGY | Cyclin D1 - metabolism | Cell Proliferation | Protein-Tyrosine Kinases - metabolism | Cyclin-Dependent Kinase 4 - genetics | Heart - physiology | Humans | Myosin Heavy Chains - genetics | Cyclin B1 - metabolism | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Myocardial Infarction - pathology | Transforming Growth Factor beta - antagonists & inhibitors | Myocardial Infarction - veterinary | Induced Pluripotent Stem Cells - cytology | Induced Pluripotent Stem Cells - metabolism | CDC2 Protein Kinase - genetics | Myocytes, Cardiac - cytology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Cyclin B1 - genetics | Rats | Mice, Transgenic | Nuclear Proteins - metabolism | Myocardial Infarction - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Cytokinesis | Regeneration | Animals | Cyclin D1 - genetics | Nuclear Proteins - antagonists & inhibitors | Myocytes, Cardiac - metabolism | Mice | Transforming Growth Factor beta - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Heart | Bone morphogenetic proteins | Transforming growth factors | Cell cycle | Stem cells | Index Medicus | Cell Cycle | Cardiomyocyte | Cell Division | Cyclin
Journal Article
Nature, ISSN 0028-0836, 02/2013, Volume 494, Issue 7438, pp. 502 - 505
Mammalian telomeres repress DNA-damage activation at natural chromosome ends by recruiting specific inhibitors of the DNA-damage machinery that form a... 
UBIQUITINATION | RECOMBINATION | MAINTENANCE | COMPLEX | REPAIR | MAMMALIAN TELOMERES | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | CELL-CYCLE | PROTEINS | TRF2 | Tumor Suppressor Proteins - antagonists & inhibitors | Chromosomes, Mammalian - genetics | Protein Multimerization | Ubiquitin-Protein Ligases - antagonists & inhibitors | Telomeric Repeat Binding Protein 2 - chemistry | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Telomere - metabolism | Protein-Serine-Threonine Kinases - metabolism | Telomere - genetics | Protein Structure, Tertiary | Endopeptidases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - metabolism | Signal Transduction | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Ataxia Telangiectasia Mutated Proteins | Endopeptidases - deficiency | Protein Transport | Animals | DNA Repair | Telomeric Repeat Binding Protein 2 - metabolism | Mice | DNA Damage | Enzyme Activation | Tumor Suppressor p53-Binding Protein 1 | Chromosomes, Mammalian - metabolism | Telomeres | Research | Binding proteins | Observations | Properties | DNA damage | Proteins | Enzymes | DNA methylation | Amino acids | Agreements | Telomerase | Chromosomes | Index Medicus | RNF168 | Brca1 | genomic stability | telomere | ATM | NHEJ
Journal Article
Nature, ISSN 0028-0836, 08/2010, Volume 466, Issue 7309, pp. 941 - 946
DNA double-strand breaks (DSBs) pose a potent threat to genome integrity. These lesions also contribute to the efficacy of radiotherapy and many cancer... 
REPAIR PROTEINS | COMPLEX | ENZYME | SPECIFICITY | STRUCTURAL BASIS | MULTIDISCIPLINARY SCIENCES | DOUBLE-STRAND BREAKS | CHAINS | MAMMALIAN-CELLS | BINDING | STATISTICAL-MODEL | Chromatin - metabolism | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | DNA Repair - physiology | Ubiquitin - metabolism | Ubiquitin-Protein Ligases - antagonists & inhibitors | DNA Breaks, Double-Stranded | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cysteine Endopeptidases - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cysteine Endopeptidases - deficiency | Ubiquitination - physiology | Protein-Serine-Threonine Kinases - metabolism | Chromatin - chemistry | Cell Line | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Ubiquitin - genetics | Ataxia Telangiectasia Mutated Proteins | Ubiquitin-Conjugating Enzymes - metabolism | Cysteine Endopeptidases - genetics | Cell Line, Tumor | Protein Binding | Ubiquitin-Conjugating Enzymes - antagonists & inhibitors | Ubiquitin-Protein Ligases - genetics | Ubiquitin | Amino acids | Genetic aspects | Models | Chemical properties | DNA damage | Proteins | Enzymes | Genetics | Mutation | DNA repair | Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 11/2014, Volume 16, Issue 12, pp. 1257 - 1264
Journal Article
Cell Reports, ISSN 2211-1247, 09/2015, Volume 12, Issue 12, pp. 1968 - 1977
Breast cancers (BCs) typically express estrogen receptors (ERs) but frequently exhibit de novo or acquired resistance to hormonal therapies. Here, we show that... 
NOTCH | ESTROGEN | ADJUVANT TAMOXIFEN | RECEPTOR | CELL BIOLOGY | Estradiol - analogs & derivatives | Receptors, Estrogen - metabolism | Neoplastic Stem Cells - drug effects | Receptors, Notch - metabolism | Homeodomain Proteins - metabolism | Humans | Retinal Dehydrogenase - metabolism | p-Aminoazobenzene - analogs & derivatives | Receptors, Notch - genetics | Receptors, Notch - antagonists & inhibitors | Basic Helix-Loop-Helix Transcription Factors - metabolism | Neoplastic Stem Cells - metabolism | Serrate-Jagged Proteins | p-Aminoazobenzene - pharmacology | Neoplastic Stem Cells - pathology | Estradiol - pharmacology | Jagged-1 Protein | Basic Helix-Loop-Helix Transcription Factors - genetics | Signal Transduction | Isoenzymes - genetics | Membrane Proteins - genetics | Cell Cycle Proteins - metabolism | Benzazepines - pharmacology | Retinal Dehydrogenase - genetics | Breast Neoplasms - drug therapy | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - genetics | Survival Analysis | Cell Line, Tumor | Retinal Dehydrogenase - antagonists & inhibitors | Mice | Calcium-Binding Proteins - genetics | Transcription Factor HES-1 | Gene Expression Regulation, Neoplastic | Cell Cycle Proteins - antagonists & inhibitors | Estrogen Receptor Antagonists - pharmacology | Intercellular Signaling Peptides and Proteins - metabolism | Isoenzymes - metabolism | Cell Cycle Proteins - genetics | Female | Membrane Proteins - metabolism | Calcium-Binding Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Receptors, Estrogen - genetics | Antineoplastic Agents, Hormonal - pharmacology | Intercellular Signaling Peptides and Proteins - genetics | Proto-Oncogene Proteins - genetics | Basic Helix-Loop-Helix Transcription Factors - antagonists & inhibitors | Homeodomain Proteins - genetics | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - pathology | Homeodomain Proteins - antagonists & inhibitors | Tamoxifen - pharmacology | Breast Neoplasms - mortality | Cell Proliferation - drug effects | Isoenzymes - antagonists & inhibitors | Receptor, Notch4 | Drug Resistance, Neoplasm - drug effects | Index Medicus | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Cancer and Oncology | Medicin och hälsovetenskap | Cancer och onkologi
Journal Article