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Journal of clinical oncology, ISSN 1527-7755, 2013, Volume 31, Issue 34, pp. 4333 - 4342
.... Patients and Methods In a series of 212 adult T-ALLs included in the multicenter randomized GRAALL-2003 and -2005 trials, we searched for additional N/K-RAS mutations and PTEN defects... 
ACTIVATION | THERAPY | NOTCH1 | PRETHYMIC PHENOTYPE | ONCOLOGY | PATHWAY | GENES | PTEN | MUTATIONS | EXPRESSION | F-Box-WD Repeat-Containing Protein 7 | Multivariate Analysis | Predictive Value of Tests | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Humans | Male | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - mortality | Young Adult | Time Factors | DNA Mutational Analysis | Gene Deletion | Cell Cycle Proteins - genetics | Adult | Female | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - therapy | PTEN Phosphohydrolase - genetics | Genetic Predisposition to Disease | Membrane Proteins - genetics | Risk Factors | Kaplan-Meier Estimate | Proportional Hazards Models | Proto-Oncogene Proteins - genetics | Disease-Free Survival | Phenotype | GTP Phosphohydrolases - genetics | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - classification | Mutation | Receptor, Notch1 - genetics | Ubiquitin-Protein Ligases - genetics | F-Box Proteins - genetics | GTP Phosphohydrolases | ras Proteins | Innate immunity | Life Sciences | F-Box Proteins | Immunology | PTEN Phosphohydrolase | Proto-Oncogene Proteins | Membrane Proteins | Ubiquitin-Protein Ligases | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma | Receptor, Notch1 | Cell Cycle Proteins
Journal Article
Genes & development, ISSN 0890-9369, 2013, Volume 27, Issue 10, pp. 1101 - 1114
...) mice and subjected them to DMBA/PMA-induced skin carcinogenesis, which depends on oncogenic Ras signaling... 
Huwe1 | c-Myc | Mule | Ras | p21 | Miz1 | DNA-DAMAGE | KERATINOCYTE GROWTH | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | BASE EXCISION-REPAIR | HUWE1 UBIQUITIN LIGASE | NEGATIVE REGULATION | GENETICS & HEREDITY | ARF TUMOR-SUPPRESSOR | DIFFERENTIATION | MIZ-1 | HUMAN CANCER | Protein Inhibitors of Activated STAT - deficiency | Tetradecanoylphorbol Acetate - pharmacology | 9,10-Dimethyl-1,2-benzanthracene - pharmacology | Male | Protein Inhibitors of Activated STAT - metabolism | Cyclin-Dependent Kinase Inhibitor p15 - biosynthesis | Oncogene Protein p21(ras) - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | Oncogene Protein p21(ras) - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Nuclear Proteins - deficiency | Protein Inhibitors of Activated STAT - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Nuclear Proteins - genetics | Protein Inhibitors of Activated STAT - antagonists & inhibitors | Skin Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis | Signal Transduction | Down-Regulation | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Skin Neoplasms - chemically induced | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Skin Neoplasms - metabolism | Keratinocytes - pathology | Animals | Tumor Suppressor Protein p53 | Keratinocytes - drug effects | Keratinocytes - metabolism | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-myc - deficiency | Skin Neoplasms - genetics | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Ubiquitin-Protein Ligases - deficiency | Mice | Proto-Oncogene Proteins c-myc - genetics | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Genes, ras | Ubiquitin-Protein Ligases - genetics | Oncogene Protein p21(ras) - genetics | Carcinogenesis | Ras genes | Analysis | Research Paper
Journal Article
Cancer cell, ISSN 1535-6108, 2014, Volume 25, Issue 2, pp. 243 - 256
.... Although it is widely accepted that acquisition of an activating mutation endows RAS genes with functional autonomy, recent studies suggest that the wild-type forms of Ras may contribute to mutant... 
ACTIVATION | INHIBITION | ONCOGENIC RAS | TUMOR PROGRESSION | CHK1 | ONCOLOGY | INITIATION | COMBINATION | SUPPRESSION | ATR | KINASES | CELL BIOLOGY | Neoplasms - metabolism | Protein Kinases - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Humans | ras Proteins - metabolism | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | GTP Phosphohydrolases - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Flow Cytometry | Neoplasms - genetics | DNA Damage - genetics | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | DNA Damage - drug effects | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Mutation - genetics | Animals | GTP Phosphohydrolases - metabolism | Membrane Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | GTP Phosphohydrolases - genetics | Mice, Nude | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Checkpoint Kinase 1 | Mice | Cell Transformation, Neoplastic - pathology | Neoplasms - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Chemotherapy | DNA damage | DNA | Genetic research | DNA repair | Cancer | Tumors
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 2017, Volume 292, Issue 31, pp. 12981 - 12993
...% conserved between the Ras isoforms. Because of their very high sequence identity, biochemical studies done on H-Ras have been considered representative of all three Ras proteins... 
EVOLUTIONARY TREE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ESCHERICHIA-COLI | enzyme catalysis | Ras protein | allosteric regulation | conformational change | oncogene | enzyme structure | P21 | PHOSPHATE | STRUCTURAL BASIS | NUCLEOTIDE-FREE | ACTIVATING PROTEINS | EXPRESSION | GTP HYDROLYSIS | CONFORMATIONAL STATES | Proto-Oncogene Proteins p21(ras) - genetics | Allosteric Regulation | Humans | Crystallography, X-Ray | Guanosine Triphosphate - metabolism | Isoenzymes - chemistry | Dinucleoside Phosphates - chemistry | GTP Phosphohydrolases - chemistry | Isoenzymes - metabolism | Proto-Oncogene Proteins c-raf - chemistry | Proto-Oncogene Proteins p21(ras) - chemistry | Guanosine Triphosphate - chemistry | Membrane Proteins - metabolism | Protein Interaction Domains and Motifs | Peptide Fragments - genetics | Proto-Oncogene Proteins p21(ras) - metabolism | Recombinant Proteins - metabolism | Catalytic Domain | Peptide Fragments - metabolism | Biocatalysis | Proto-Oncogene Proteins c-raf - genetics | Isoenzymes - genetics | Membrane Proteins - genetics | Enzyme Stability | Guanosine Triphosphate - analogs & derivatives | Models, Molecular | Recombinant Proteins - chemistry | Dinucleoside Phosphates - metabolism | Proto-Oncogene Proteins c-raf - metabolism | Point Mutation | Peptide Fragments - chemistry | GTP Phosphohydrolases - metabolism | Membrane Proteins - chemistry | GTP Phosphohydrolases - genetics | Allosteric Site | Ligands | Protein Conformation | Amino Acid Substitution | Enzymology
Journal Article
Aging cell, ISSN 1474-9718, 2017, Volume 16, Issue 5, pp. 1094 - 1103
.... In this study, we have shown that both Akt and p21 are required to induce cellular senescence in response to p53 expression. In a p53... 
senescence | NOX4 | Akt | reactive oxygen species | p53 | CELLS | ACTIVATION | P53-INDUCED SENESCENCE | MTOR | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | OVEREXPRESSION | INHIBITION | ONCOGENIC RAS | GROWTH ARREST | ACCUMULATION | Interleukin-8 - genetics | RNA, Small Interfering - genetics | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Tumor Suppressor Protein p53 - antagonists & inhibitors | Proto-Oncogene Proteins p21(ras) - genetics | Epithelial Cells - drug effects | Humans | Cellular Senescence - drug effects | NF-kappa B - metabolism | Proto-Oncogene Proteins c-akt - genetics | Tumor Suppressor Protein p53 - genetics | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Cycle Checkpoints - genetics | Interleukin-8 - metabolism | Epithelial Cells - cytology | Mechanistic Target of Rapamycin Complex 2 - genetics | Proto-Oncogene Proteins c-akt - metabolism | Interleukin-6 - metabolism | Fibroblasts - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Lymphocytes - metabolism | Cellular Senescence - genetics | Promoter Regions, Genetic | NADPH Oxidase 4 - genetics | Interleukin-6 - genetics | Signal Transduction | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - antagonists & inhibitors | Lymphocytes - cytology | Morpholines | Mechanistic Target of Rapamycin Complex 2 - metabolism | NADPH Oxidase 4 - metabolism | NF-kappa B - genetics | Cell Cycle Checkpoints - drug effects | Fibroblasts - drug effects | Lymphocytes - drug effects | Cell Line, Tumor | Protein Binding | Fibroblasts - cytology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Chromones | RNA, Small Interfering - metabolism | Tumor proteins | Analysis | TOR protein | NF-κB protein | Senescence | H-Ras protein | p53 Protein | Homeostasis | AKT protein | Rapamycin | Interleukin 6 | Signal transduction | Cyclin-dependent kinase inhibitor p21 | NOX4 protein | Cell cycle | Fibroblasts | Interleukin 8 | Original
Journal Article
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 02/2015, Volume 290, Issue 8, pp. 4908 - 4927
synGAP is a neuron-specific Ras and Rap GTPase-activating protein (GAP) found in high concentrations in the postsynaptic density (PSD... 
NMDA RECEPTOR | DOMAIN | STIMULATION | INHIBITION | CALPAIN | CLONING | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTATIONS | HIPPOCAMPAL-NEURONS | PLASTICITY | Oncogene Proteins - genetics | ras Proteins - genetics | Phosphorylation | ras GTPase-Activating Proteins - chemistry | rap1 GTP-Binding Proteins - chemistry | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Receptors, N-Methyl-D-Aspartate - metabolism | ras Proteins - metabolism | Neurons - cytology | GTPase-Activating Proteins - metabolism | Receptors, N-Methyl-D-Aspartate - genetics | Cyclin-Dependent Kinase 5 - chemistry | Cyclin-Dependent Kinase 5 - genetics | ras GTPase-Activating Proteins - genetics | Receptors, N-Methyl-D-Aspartate - chemistry | ras Proteins - chemistry | Proto-Oncogene Proteins p21(ras) - chemistry | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | rap1 GTP-Binding Proteins - metabolism | ras GTPase-Activating Proteins - metabolism | Oncogene Proteins - chemistry | Cells, Cultured | Oncogene Proteins - metabolism | Rats | Synapses - enzymology | GTPase-Activating Proteins - chemistry | Cyclin-Dependent Kinase 5 - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Animals | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - chemistry | Neurons - enzymology | GTPase-Activating Proteins - genetics | rap1 GTP-Binding Proteins - genetics | rap GTP-Binding Proteins | Ras Protein | Ras-related Protein 1 (Rap1) | Postsynaptic Density | Ca2 | Synaptic Plasticity | Small GTPase | Neurobiology | Mass Spectrometry (MS) | Cyclin-dependent Kinase 5 (CDK5) | Protein Kinase | Calmodulin-dependent Protein Kinase II (CaMKII) | Synaptic GTPase-activating Protein (synGAP)
Journal Article
Nature (London), ISSN 1476-4687, 2013, Volume 496, Issue 7443, pp. 101 - 105
Cancer cells have metabolic dependencies that distinguish them from their normal counterparts(1). Among these dependencies is an increased use of the amino... 
GLUCOSE | MULTIDISCIPLINARY SCIENCES | MASS-SPECTROMETRY | ADDICTION | TRANSFORMED-CELLS | Care and treatment | Pancreatic cancer | Physiological aspects | Development and progression | Research | Health aspects | Guanosine triphosphatase | Glutamine | Cancer | Enzymes | Oxidative stress | Glucose | Metabolites | Cancer therapies
Journal Article
The New England journal of medicine, ISSN 1533-4406, 2013, Volume 369, Issue 11, pp. 1023 - 1034
Journal Article
Immunity (Cambridge, Mass.), ISSN 1074-7613, 2017, Volume 47, Issue 6, pp. 1083 - 1099.e6
.... We report that oncogenic RAS signaling can upregulate tumor cell PD-L1 expression through a mechanism involving increases in PD-L1 mRNA stability via modulation of the AU-rich element-binding protein tristetraprolin (TTP... 
PD-L1 | TTP | KRAS | RAS | tristetraprolin | immunotherapy | CELL LUNG-CANCER | ACTIVATED PROTEIN-KINASE | EPITHELIAL-CELLS | TRISTETRAPROLIN | MELANOMA-CELLS | TNF-ALPHA | IMMUNOLOGY | EXPRESSION | CHECKPOINT BLOCKADE | Proto-Oncogene Proteins p21(ras) - immunology | Neoplasm Transplantation | RNA, Messenger - immunology | Tumor Escape | Proto-Oncogene Proteins p21(ras) - genetics | Tristetraprolin - immunology | Colorectal Neoplasms - genetics | Humans | Gene Expression Regulation, Neoplastic | Intracellular Signaling Peptides and Proteins - immunology | Lung Neoplasms - pathology | Male | Female | Intracellular Signaling Peptides and Proteins - genetics | Lung Neoplasms - genetics | Signal Transduction | MAP Kinase Kinase Kinases - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Protein-Serine-Threonine Kinases - genetics | Epithelial Cells - pathology | RNA Cleavage | RNA Stability | B7-H1 Antigen - genetics | B7-H1 Antigen - immunology | MAP Kinase Kinase Kinases - immunology | Lung Neoplasms - immunology | Animals | Colorectal Neoplasms - immunology | Tristetraprolin - genetics | Epithelial Cells - immunology | Cell Line, Tumor | Protein Binding | Protein-Serine-Threonine Kinases - immunology | Mice | Mice, Inbred BALB C | Colorectal Neoplasms - pathology | Messenger RNA | Gastrointestinal diseases | Immunotherapy | Colorectal cancer | Cellular signal transduction | Cancer | Protein binding | Transcription factors | Phosphorylation | Lung cancer | Genomes | Kinases | Proteins | Signal transduction | Restoration | DNA methylation | Tumor necrosis factor-TNF | Oncogenes | Immune system | Cytokines | Ras protein | Ribonucleic acid--RNA | Gene expression | Patients | Signaling | Immunosuppression | 3' Untranslated regions | Ligands | Protein expression | Mutation | Tumors
Journal Article