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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 | 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
Nature (London), ISSN 1476-4687, 2018, Volume 562, Issue 7725, pp. 69 - 75
Primary liver cancer represents a major health problem. It comprises hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), which differ... 
PATHOGENESIS | HEPATOCELLULAR-CARCINOMA | READ ALIGNMENT | HEPATOCYTES | DNA | INFLAMMATION | PACKAGE | MULTIDISCIPLINARY SCIENCES | FRAMEWORK | BINDING | DISCOVERY | Humans | Tumor Microenvironment | Apoptosis - genetics | Hepatocytes - pathology | Male | Gene Expression Profiling | Genes, myc | Hepatocytes - metabolism | Proto-Oncogene Proteins c-akt - genetics | DNA-Binding Proteins - metabolism | Carcinoma, Hepatocellular - genetics | DNA Transposable Elements - genetics | Female | Liver Neoplasms - pathology | Cell Differentiation | Cell Lineage - genetics | Disease Models, Animal | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Cytokines - metabolism | Liver Neoplasms - genetics | Carcinogenesis - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Transcription Factors - metabolism | Cholangiocarcinoma - pathology | Animals | Epigenesis, Genetic - genetics | Carcinoma, Hepatocellular - pathology | Cholangiocarcinoma - genetics | Mosaicism | Mice | Necrosis - genetics | Genes, ras | Liver cancer | Research | Carcinogenesis | Oncology, Experimental | Apoptosis | Cancer | Animal models | Cytokines | Liver | Hepatocellular carcinoma | Genomes | Metastasis | Risk analysis | Gene expression | Risk factors | Metastases | Hepatocytes | Morphology | DNA methylation | Tumorigenesis | Bioinformatics | Cholangiocarcinoma | Deoxyribonucleic acid--DNA | Tumors | T-Box Domain Proteins/metabolism | Hepatocytes/pathology | DNA-Binding Proteins/metabolism | Life Sciences | Cholangiocarcinoma/pathology | Transcription Factors/metabolism | Necrosis/genetics | Cytokines/metabolism | Epigenesis, Genetic/genetics | Cyclin-Dependent Kinase Inhibitor p16/deficiency | Carcinoma, Hepatocellular/pathology | DNA Transposable Elements/genetics | Cell Lineage/genetics | T-Box Domain Proteins/genetics | Transcription Factors/genetics | Apoptosis/genetics | Proto-Oncogene Proteins c-akt/genetics | Liver Neoplasms/genetics | Cholangiocarcinoma/genetics | Liver Neoplasms/pathology | DNA-Binding Proteins/genetics | Hepatocytes/metabolism | Carcinoma, Hepatocellular/genetics | Carcinogenesis/genetics
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 08/2005, Volume 25, Issue 16, pp. 6964 - 6979
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
TRANSCRIPTIONAL ACTIVATION | ACTIVATED PROTEIN-KINASE | CBP-INDUCED STIMULATION | EARLY GENE-PRODUCTS | PROTEASOMAL DEGRADATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | TRANSFORMING ACTIVITY | TERMINAL TRANSACTIVATION DOMAIN | SUMO-1 MODIFICATION | BINDING PROTEIN | CELL BIOLOGY | Phosphorylation | Threonine - chemistry | Immunoprecipitation | Luciferases - metabolism | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Immunoblotting | Transcription Factor AP-1 - metabolism | Transfection | Time Factors | Proto-Oncogene Proteins c-jun - chemistry | Transcription, Genetic | Binding Sites | Dimerization | Proto-Oncogene Proteins p21(ras) - metabolism | Protein Structure, Tertiary | Mutagenesis, Site-Directed | Small Ubiquitin-Related Modifier Proteins - metabolism | Down-Regulation | Proto-Oncogene Proteins c-fos - metabolism | Glutathione Transferase - metabolism | Recombinant Fusion Proteins - chemistry | Transcription Factor AP-1 - chemistry | Mitogen-Activated Protein Kinase 3 - metabolism | Proto-Oncogene Proteins c-jun - metabolism | Protein Binding | SUMO-1 Protein - metabolism | HeLa Cells | Kinetics | Lysine - chemistry | Subcellular Fractions | Microscopy, Fluorescence | Mitogen-Activated Protein Kinase 1 - metabolism | Life Sciences | Biochemistry, Molecular Biology | Gene Expression
Journal Article
Nature cell biology, ISSN 1476-4679, 2011, Volume 13, Issue 9, pp. 1108 - 1115
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 01/2016, Volume 291, Issue 3, pp. 1014 - 1027
The majority of biosynthetic secretory proteins initiate their journey through the endomembrane system from specific sub-domains of the endoplasmic reticulum... 
COAT | COMPLEX | TRANSPORT | CAENORHABDITIS-ELEGANS | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | COPII VESICLE FORMATION | ENDOPLASMIC-RETICULUM | ER | BINDING | INSIGHTS | Vesicular Transport Proteins - metabolism | Caenorhabditis elegans Proteins - chemistry | Humans | Membrane Microdomains - ultrastructure | Endoplasmic Reticulum - ultrastructure | GTP Phosphohydrolases - chemistry | Caenorhabditis elegans - physiology | ras GTPase-Activating Proteins - genetics | Vesicular Transport Proteins - antagonists & inhibitors | RNA Interference | ras GTPase-Activating Proteins - metabolism | Enzyme Inhibitors - pharmacology | COP-Coated Vesicles - metabolism | Recombinant Proteins - chemistry | Guanylyl Imidodiphosphate - pharmacology | Receptor Protein-Tyrosine Kinases - metabolism | Monomeric GTP-Binding Proteins - antagonists & inhibitors | Caenorhabditis elegans - ultrastructure | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Models, Biological | Monomeric GTP-Binding Proteins - chemistry | GTPase-Activating Proteins - genetics | Mutation | Caenorhabditis elegans Proteins - genetics | Caenorhabditis elegans - enzymology | Membrane Microdomains - metabolism | Caenorhabditis elegans Proteins - metabolism | Endoplasmic Reticulum - metabolism | Guanosine Triphosphate - metabolism | GTP Phosphohydrolases - antagonists & inhibitors | GTPase-Activating Proteins - metabolism | Microscopy, Atomic Force | Organelle Shape - drug effects | Recombinant Proteins - metabolism | COP-Coated Vesicles - ultrastructure | GTPase-Activating Proteins - antagonists & inhibitors | Vesicular Transport Proteins - genetics | COP-Coated Vesicles - drug effects | Monomeric GTP-Binding Proteins - genetics | Animals | Caenorhabditis elegans - drug effects | Caenorhabditis elegans Proteins - antagonists & inhibitors | Monomeric GTP-Binding Proteins - metabolism | Receptor Protein-Tyrosine Kinases - genetics | Membrane Microdomains - drug effects | Lipid Bilayers - chemistry | Lipid Bilayers - metabolism | Amino Acid Substitution | COPII | membrane transport | endoplasmic reticulum (ER) | GTPase | membrane bilayer | Cell Biology
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2004, Volume 101, Issue 37, pp. 13489 - 13494
Tuberous sclerosis complex (TSC) is a genetic disorder caused by mutations in either of the two tumor suppressor genes TSC1 or TSC2, which encode hamartin and... 
Proteins | Phorbol esters | Biological Sciences | Phosphorylation | Cell growth | HEK293 cells | Roux | Tuberous sclerosis | Antibodies | Insulin | Tumors | MAMMALIAN TARGET | PROTEIN | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | PHOSPHOINOSITIDE 3-KINASE/AKT PATHWAY | GENE-PRODUCTS | TSC1 | CELL-GROWTH | IDENTIFICATION | HETEROZYGOSITY | MTOR | Protein Kinases - metabolism | Tetradecanoylphorbol Acetate - pharmacology | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Molecular Sequence Data | Tetradecanoylphorbol Acetate - analogs & derivatives | Phosphatidylinositol 3-Kinases - metabolism | Oncogene Protein p21(ras) - metabolism | MAP Kinase Signaling System | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Amino Acid Sequence | Cell Line | Repressor Proteins - chemistry | Tumor Suppressor Proteins - metabolism | Repressor Proteins - genetics | Serine - genetics | Mutation - genetics | Phosphoserine - metabolism | Tuberous Sclerosis - enzymology | Serine - metabolism | Tuberous Sclerosis - genetics | Proteins - genetics | Proto-Oncogene Proteins c-akt | Animals | Proteins - metabolism | Tuberous Sclerosis - metabolism | Models, Biological | Protein Binding | TOR Serine-Threonine Kinases | Enzyme Activation | Proteins - antagonists & inhibitors | Oncogene Protein p21(ras) - genetics | Esters | Research
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 10/2001, Volume 21, Issue 19, pp. 6706 - 6717
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
SIGNAL-TRANSDUCTION | ACTIVATED PROTEIN-KINASE | ONCOGENIC RAS | INDUCED APOPTOSIS | PHOSPHATIDYLINOSITOL 3-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | B-RAF | GROWTH-FACTOR | CELL-CYCLE PROGRESSION | INDEPENDENT PATHWAYS | SERINE/THREONINE KINASE | CELL BIOLOGY | MAP Kinase Kinase 1 | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Nucleus - metabolism | Extracellular Matrix - physiology | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | rho GTP-Binding Proteins - genetics | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Proto-Oncogene Proteins - genetics | cdc42 GTP-Binding Protein - physiology | rho GTP-Binding Proteins - physiology | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins c-akt | Animals | rac1 GTP-Binding Protein - physiology | cdc42 GTP-Binding Protein - genetics | Proto-Oncogene Proteins - physiology | Anoikis | Fibroblasts - cytology | Mice | Mutation | Mitogen-Activated Protein Kinase 3 | Apoptosis | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | rac1 GTP-Binding Protein - genetics | Protein-Serine-Threonine Kinases | Biodiversity | Cellular Biology | Embryology and Organogenesis | Life Sciences | Mitogen-Activated Protein Kinase Kinases | Fibroblasts | Proto-Oncogene Proteins | Subcellular Processes | Mitogen-Activated Protein Kinases | Proto-Oncogene Proteins c-raf | Extracellular Matrix | Biochemistry, Molecular Biology | Systematics, Phylogenetics and taxonomy | Tumor Suppressor Protein p53 | cdc42 GTP-Binding Protein | Development Biology | rac1 GTP-Binding Protein | Mitogen-Activated Protein Kinase 1 | Molecular biology | rho GTP-Binding Proteins | Cell Nucleus | Cancer | Cell Growth and Development
Journal Article
Nature cell biology, ISSN 1476-4679, 2005, Volume 7, Issue 8, pp. 837 - 843
Ras proteins control the signalling pathways that are responsible for normal growth and malignant transformation... 
RECRUITMENT | CHOLESTEROL | MEMBRANE | 14-3-3 BINDING | KINASE | C-RAF | TARGETS | CAVEOLAE | FAMILY | CELL BIOLOGY | RNA, Small Interfering - genetics | MAP Kinase Signaling System - physiology | Tetradecanoylphorbol Acetate - pharmacology | Cadherins - metabolism | Epithelial Cells - drug effects | Humans | ras Proteins - metabolism | Cell Shape - genetics | raf Kinases - metabolism | Cell Movement - genetics | Cell Movement - physiology | Repressor Proteins - physiology | Epithelial Cells - physiology | Mitogen-Activated Protein Kinase Kinases - metabolism | Transfection | Cytoskeletal Proteins - metabolism | Flavonoids - pharmacology | Phosphorylation - drug effects | raf Kinases - genetics | ras Proteins - physiology | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Microscopy, Electron, Transmission | Cell Adhesion - genetics | Microscopy, Electron, Scanning | Proto-Oncogene Proteins c-raf - genetics | beta Catenin | Caveolae - metabolism | Enzyme Inhibitors - pharmacology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Epithelial Cells - ultrastructure | Repressor Proteins - genetics | Cell Adhesion - drug effects | Proto-Oncogene Proteins c-raf - metabolism | 14-3-3 Proteins - metabolism | Cell Shape - drug effects | Proto-Oncogene Proteins c-akt | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Line, Tumor | Protein Binding | Cytosol - metabolism | Trans-Activators - metabolism | Epidermal Growth Factor - pharmacology | HeLa Cells | Mitogen-Activated Protein Kinase 1 - metabolism | Ras genes | Physiological aspects | Genetic aspects | Cellular signal transduction | Research | Identification and classification | Cell migration
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 02/2016, Volume 291, Issue 9, pp. 4589 - 4602
.... In response to netrin-1 stimulation, DCC becomes a signaling platform to recruit proteins that promote axon outgrowth and guidance... 
CARGO RECOGNITION | TYROSINE PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | GAP | GROWTH | RAS P21 | RECEPTOR | FOCAL ADHESION KINASE | C-TERMINAL DOMAIN | GTPASE-ACTIVATING PROTEIN | COLORECTAL-CANCER DCC | Humans | Nerve Growth Factors - metabolism | p120 GTPase Activating Protein - chemistry | RNA Interference | Tumor Suppressor Proteins - chemistry | Neurons - metabolism | Peptide Fragments - genetics | DCC Receptor | Tumor Suppressor Proteins - metabolism | Signal Transduction | Rats | Recombinant Proteins - chemistry | Recombinant Fusion Proteins - chemistry | p120 GTPase Activating Protein - antagonists & inhibitors | Peptide Fragments - chemistry | Embryo, Mammalian - cytology | Nerve Growth Factors - genetics | Peptide Fragments - antagonists & inhibitors | Chickens | Mutant Proteins - agonists | Tumor Suppressor Proteins - antagonists & inhibitors | p120 GTPase Activating Protein - metabolism | Netrin-1 | Neurons - cytology | p120 GTPase Activating Protein - genetics | Cerebral Cortex - cytology | Recombinant Fusion Proteins - metabolism | Cerebral Cortex - metabolism | Nerve Tissue Proteins - chemistry | Glutathione Transferase - genetics | Tumor Suppressor Proteins - genetics | HEK293 Cells | Receptors, Cell Surface - chemistry | Protein Interaction Domains and Motifs | Recombinant Proteins - metabolism | Nerve Tissue Proteins - antagonists & inhibitors | Peptide Fragments - metabolism | Cells, Cultured | Mutant Proteins - genetics | Receptors, Cell Surface - agonists | Axons - metabolism | Glutathione Transferase - metabolism | Receptors, Cell Surface - metabolism | Mutant Proteins - metabolism | Nerve Growth Factors - chemistry | Nerve Tissue Proteins - genetics | Protein Transport | Nerve Tissue Proteins - metabolism | Animals | Nerve Growth Factors - antagonists & inhibitors | Tumor Suppressor Proteins - agonists | Amino Acid Substitution | neurodevelopment | signal transduction | DCC | Neurobiology | Ras protein | neurite outgrowth | netrin-1
Journal Article
The Journal of immunology (1950), ISSN 1550-6606, 2009, Volume 183, Issue 8, pp. 4879 - 4886
...) in the receptor's cytoplasmic region. The adaptor protein downstream of tyrosine kinase 2 (Dok2) bound directly to the phosphorylated NPLY motif with a 10-fold higher affinity... 
STEM-CELLS | ACTIVATION | PROGNOSTIC-FACTOR | INHIBITION | DOCKING PROTEIN | PHOSPHORYLATION | NEGATIVE REGULATION | MACROPHAGES | DOWN-REGULATION | SURFACE-PROTEINS | IMMUNOLOGY | Phosphoproteins - immunology | Antigens, CD - immunology | p120 GTPase Activating Protein - metabolism | Humans | Glycoproteins - metabolism | p120 GTPase Activating Protein - genetics | Phosphoproteins - metabolism | Antigens, CD - metabolism | Gene Knockdown Techniques | DNA-Binding Proteins - metabolism | Matrilin Proteins | Signal Transduction - immunology | ras GTPase-Activating Proteins - genetics | Interleukin-4 - pharmacology | RNA, Small Interfering - immunology | Myeloid Cells - immunology | Adaptor Proteins, Signal Transducing - immunology | Antigens, Surface - metabolism | Myeloid Cells - drug effects | Interleukin-8 - metabolism | Extracellular Matrix Proteins - metabolism | Macrophages - immunology | ras GTPase-Activating Proteins - metabolism | DNA-Binding Proteins - immunology | Cartilage Oligomeric Matrix Protein | RNA-Binding Proteins - immunology | Antigens, Surface - genetics | Rats | Receptors, Cell Surface - metabolism | Phosphoproteins - genetics | Receptors, Cell Surface - immunology | Glycoproteins - immunology | Macrophages - metabolism | Animals | Extracellular Matrix Proteins - immunology | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Myeloid Cells - metabolism | Macrophages - drug effects | Mice | ras GTPase-Activating Proteins - immunology | Adaptor Proteins, Signal Transducing - metabolism | Interleukin-8 - immunology | Antigens, Surface - immunology | RNA-Binding Proteins - metabolism | RNA, Small Interfering - metabolism | Receptors, Cell Surface - genetics
Journal Article
Journal Article
Current biology, ISSN 0960-9822, 2010, Volume 20, Issue 18, pp. 1654 - 1659
...]. GTPase-activating proteins (GAPs) promote GTP hydrolysis to inactivate the Rab. GEFs are thus critical activators of fusion reactions [3, 4... 
ACTIVATION | NUCLEOTIDE EXCHANGE | TRANSPORT PATHWAY | PROTEIN | STRUCTURAL BASIS |