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Cell, ISSN 0092-8674, 2007, Volume 129, Issue 7, pp. 1415 - 1426
Protein kinases control cellular decision processes by phosphorylating specific substrates. Thousands of in vivo phosphorylation sites have been identified,... 
CELLBIO | ACTIVATION | DNA-DAMAGE RESPONSE | 53BP1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | SPECTROMETRY-BASED PROTEOMICS | ATM | EUKARYOTIC PROTEINS | PROTEIN-PHOSPHORYLATION | MASS-SPECTROMETRY | SIGNALING NETWORKS | CELL BIOLOGY | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Humans | DNA Repair Enzymes - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Phosphoproteins - metabolism | CDC2 Protein Kinase - metabolism | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | DNA Repair Enzymes - metabolism | Cell Cycle Proteins - genetics | DNA Damage - genetics | Proteomics - methods | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | CDC2 Protein Kinase - genetics | Computational Biology - methods | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Repressor Proteins - genetics | Ataxia Telangiectasia Mutated Proteins | Binding Sites - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Glycogen Synthase Kinase 3 - genetics | Signal Transduction - physiology | Software | Tumor Suppressor p53-Binding Protein 1
Journal Article
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
Journal Article
Cell Reports, ISSN 2211-1247, 12/2015, Volume 13, Issue 11, pp. 2425 - 2439
To identify therapeutic targets for glioblastoma (GBM), we performed genome-wide CRISPR-Cas9 knockout (KO) screens in patient-derived GBM stem-like cells... 
WEE1 | CRISPR-Cas9 | Glioblastoma | cancer therapeutics | functional genomics | PKMYT1 | gene editing | Myt1 | Cancer therapeutics | Gene editing | Functional genomics | ACTIVATION | PROTEIN | GENE-EXPRESSION | GOLGI | PHOSPHORYLATES CDC2 | HUMAN MYT1 | INHIBITORY KINASE | BRAIN | RNAI SCREEN | REQUIREMENT | 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 | Receptor, Epidermal Growth Factor - metabolism | 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 | Gene Library | CDC2 Protein Kinase - antagonists & inhibitors | Membrane Proteins - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | 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
Journal Article
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
Journal of Cell Biology, ISSN 0021-9525, 09/2012, Volume 198, Issue 6, pp. 981 - 990
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2015, Volume 10, Issue 7, p. e0130748
The activity of Cdc2 (CDK1) kinase, which coordinates cell cycle progression and DNA break repair, is blocked upon its phosphorylation at tyrosine 15 (Y15) by... 
GEL-ELECTROPHORESIS | MITOSIS | ACTIVATING KINASE | TYROSINE PHOSPHORYLATION | CDK REGULATION | WEE1 PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | P34CDC2 KINASE | S-PHASE | CHECKPOINT | SCHIZOSACCHAROMYCES-POMBE | Protein Kinases - metabolism | Schizosaccharomyces pombe Proteins - chemistry | Phosphorylation | Protein Kinases - genetics | Protein-Tyrosine Kinases - metabolism | Molecular Sequence Data | CDC2 Protein Kinase - metabolism | Schizosaccharomyces - genetics | Protein-Tyrosine Kinases - genetics | Cyclin B - genetics | Protein Isoforms - metabolism | Protein Isoforms - chemistry | Schizosaccharomyces pombe Proteins - metabolism | Cell Cycle Proteins - genetics | CDC2 Protein Kinase - chemistry | Nuclear Proteins - genetics | Amino Acid Sequence | CDC2 Protein Kinase - genetics | Schizosaccharomyces pombe Proteins - genetics | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Schizosaccharomyces - metabolism | Cell Cycle | Protein Binding | Checkpoint Kinase 1 | Cyclin B - metabolism | Protein Processing, Post-Translational | DNA Damage | Protein Isoforms - genetics | Amino acids | DNA repair | DNA damage | DNA | Cells | Cell cycle | Tyrosine | Cdc2 protein | Yeast | Threonine | CHK1 protein | Pools | Kinases | Cyclin B | S phase | Mutation | Isoelectric focusing | Inhibition | Aberration | Lesions | Damage | Repair | Binding sites | Deoxyribonucleic acid--DNA | Deoxyribonucleic acid
Journal Article
Immunologic Research, ISSN 0257-277X, 10/2011, Volume 51, Issue 1, pp. 45 - 60
Complement system activation plays an important role in both innate and acquired immunity. Activation of the complement and the subsequent formation of C5b-9... 
Allergology | Signal transduction | Immunology | Medicine & Public Health | Cell cycle | Internal Medicine | Membrane attack complex | C5b-9 terminal complement complex | Transcriptional regulation | Medicine/Public Health, general | Apoptosis | ACTIVATED PROTEIN-KINASE | SYSTEMIC LUPUS-ERYTHEMATOSUS | GUILLAIN-BARRE-SYNDROME | ULCERATIVE-COLITIS | GLOMERULAR EPITHELIAL-CELLS | C5B-9 COMPLEX | IMMUNOLOGY | S-PROTEIN | MANNAN-BINDING LECTIN | ACUTE MYOCARDIAL-INFARCTION | SMOOTH-MUSCLE-CELLS | Forkhead Transcription Factors - immunology | CDC2 Protein Kinase | Complement Membrane Attack Complex - metabolism | Cyclin-Dependent Kinase 4 - genetics | Humans | Caspase 8 - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Complement Membrane Attack Complex - immunology | MAP Kinase Signaling System - immunology | Phosphatidylinositol 3-Kinases - immunology | Cell Cycle Proteins - immunology | Cyclin B - immunology | Forkhead Transcription Factors - metabolism | Muscle Proteins - metabolism | bcl-Associated Death Protein - metabolism | Cell Membrane - metabolism | Phosphorylation - immunology | Cyclin-Dependent Kinases | Proto-Oncogene Proteins c-akt - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | Cyclin-Dependent Kinase 2 - metabolism | Mitogen-Activated Protein Kinase 3 - immunology | Muscle Proteins - immunology | G1 Phase - immunology | S Phase - immunology | Nerve Tissue Proteins - immunology | Cell Cycle Proteins - metabolism | bcl-Associated Death Protein - immunology | Cyclin-Dependent Kinase 4 - metabolism | Nerve Tissue Proteins - metabolism | Caspase 8 - immunology | Animals | Apoptosis - immunology | Proto-Oncogene Proteins c-akt - immunology | Mitogen-Activated Protein Kinase 3 - metabolism | BH3 Interacting Domain Death Agonist Protein - immunology | Cyclin B - metabolism | Cell Membrane - immunology | Forkhead Box Protein O1 | Cyclin-Dependent Kinase 2 - immunology | Medical colleges | Membranes | Immune system | apoptosis | membrane attack complex | cell cycle | signal transduction | transcriptional regulation
Journal Article
Journal Article
Nature Cell Biology, ISSN 1465-7392, 2009, Volume 11, Issue 5, pp. 644 - 651
Journal Article
Oncogene, ISSN 0950-9232, 02/2019, Volume 38, Issue 7, pp. 998 - 1018
Cell cycle regulation, especially faithful DNA replication and mitosis, are crucial to maintain genome stability. Cyclin-dependent kinase (CDK)/cyclin... 
HOLLIDAY JUNCTION RESOLUTION | INHIBITORY PHOSPHORYLATION | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | RE-REPLICATION | CYCLIN-DEPENDENT KINASE | G2 CHECKPOINT | CELL BIOLOGY | NUCLEAR ACCUMULATION | WEE1 KINASE | DNA-DAMAGE CHECKPOINT | ONCOLOGY | GENETICS & HEREDITY | CELL-CYCLE | Mitosis | Protein-Tyrosine Kinases - metabolism | Embryo Loss - enzymology | Mutation, Missense | CDC2 Protein Kinase - metabolism | DNA-Binding Proteins - metabolism | Protein-Tyrosine Kinases - genetics | Embryo Loss - pathology | S Phase | Cell Cycle Proteins - genetics | Embryo, Mammalian - enzymology | Embryo Loss - genetics | Nuclear Proteins - genetics | CDC2 Protein Kinase - genetics | Embryo, Mammalian - pathology | Cell Cycle Proteins - metabolism | Mice, Transgenic | Nuclear Proteins - metabolism | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | Animals | Mice | Enzyme Activation | Amino Acid Substitution | DNA replication | DNA damage | Analysis | Genomics | Clinical trials | Development and progression | Tumor proteins | Cell proliferation | Phosphorylation | p53 Protein | Cyclin-dependent kinases | Liver | Genomes | Lethality | Embryo fibroblasts | Kinases | Embryos | DNA biosynthesis | Cyclin-dependent kinase | Cyclin-dependent kinase 2 | S phase | Cell cycle | Endonuclease | Deoxyribonucleic acid--DNA | Cancer | Cancer models | Embryo Loss/enzymology | Protein-Tyrosine Kinases/genetics | Transcription Factors/genetics | DNA-Binding Proteins/genetics | Embryo, Mammalian/enzymology | Cell Cycle Proteins/genetics | Nuclear Proteins/genetics | CDC2 Protein Kinase/genetics
Journal Article