X
Search Filters
Format Format
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
humans (10610) 10610
animals (5660) 5660
female (4534) 4534
oncology (4510) 4510
mutation (4365) 4365
proto-oncogene proteins p21 - genetics (4064) 4064
male (3901) 3901
proto-oncogene proteins p21 (3494) 3494
proto-oncogene proteins - genetics (3464) 3464
mice (3440) 3440
cancer (3018) 3018
middle aged (2868) 2868
ras proteins - genetics (2734) 2734
proto-oncogene proteins p21 - metabolism (2681) 2681
aged (2571) 2571
biochemistry & molecular biology (2432) 2432
cell biology (2431) 2431
signal transduction (2233) 2233
adult (2078) 2078
cell line, tumor (2008) 2008
expression (1974) 1974
colorectal neoplasms - genetics (1669) 1669
tumors (1665) 1665
apoptosis (1609) 1609
genetic aspects (1580) 1580
kras (1498) 1498
phosphorylation (1466) 1466
research (1446) 1446
colorectal cancer (1385) 1385
proto-oncogene proteins - metabolism (1370) 1370
aged, 80 and over (1355) 1355
activation (1345) 1345
proto-oncogene proteins b-raf - genetics (1332) 1332
prognosis (1331) 1331
lung neoplasms - genetics (1285) 1285
proteins (1282) 1282
colorectal neoplasms - pathology (1189) 1189
gene expression regulation, neoplastic (1128) 1128
gene expression (1109) 1109
analysis (1090) 1090
pathology (1027) 1027
research article (1027) 1027
mutations (1020) 1020
cell line (1014) 1014
cell proliferation (1007) 1007
chemotherapy (995) 995
genes, ras (995) 995
ras (994) 994
rats (979) 979
adenocarcinoma - genetics (971) 971
immunohistochemistry (956) 956
multidisciplinary sciences (918) 918
metastasis (902) 902
lung neoplasms - pathology (899) 899
dna mutational analysis (888) 888
genetics & heredity (869) 869
transfection (859) 859
gene (852) 852
tumor suppressor protein p53 - genetics (850) 850
molecular sequence data (847) 847
mutation - genetics (840) 840
kinases (836) 836
growth (835) 835
adenocarcinoma (831) 831
cetuximab (831) 831
cells, cultured (819) 819
proto-oncogene proteins c-akt - metabolism (818) 818
survival (802) 802
carcinoma (795) 795
colorectal neoplasms - drug therapy (788) 788
cells (787) 787
cell cycle (769) 769
p53 (767) 767
biomarkers, tumor - genetics (748) 748
k-ras (738) 738
oncogenes (732) 732
genes (731) 731
ras proteins - metabolism (719) 719
tumor cells, cultured (718) 718
tumor suppressor protein p53 - metabolism (718) 718
base sequence (713) 713
health aspects (713) 713
lung cancer (712) 712
neoplasms (707) 707
care and treatment (703) 703
neoplasm staging (692) 692
signal transduction - drug effects (688) 688
adenocarcinoma - pathology (687) 687
receptor, epidermal growth factor - genetics (683) 683
gene mutations (672) 672
apoptosis - drug effects (671) 671
polymerase chain reaction (649) 649
antineoplastic agents - therapeutic use (648) 648
antineoplastic agents - pharmacology (647) 647
pancreatic neoplasms - genetics (646) 646
carcinoma, non-small-cell lung - genetics (645) 645
protein (637) 637
digestive system diseases (620) 620
amino acid sequence (614) 614
phenotype (610) 610
more...
Library Location Library Location
Language Language
Language Language
X
Sort by Item Count (A-Z)
Filter by Count
English (13282) 13282
Chinese (141) 141
Japanese (113) 113
German (35) 35
French (34) 34
Russian (29) 29
Spanish (11) 11
Czech (8) 8
Hungarian (8) 8
Hebrew (5) 5
Polish (4) 4
Portuguese (4) 4
Dutch (2) 2
Italian (2) 2
Croatian (1) 1
Finnish (1) 1
Swedish (1) 1
Turkish (1) 1
more...
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Journal Article
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
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
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
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2019, Volume 116, Issue 7, pp. 2551 - 2560
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 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
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
The New England journal of medicine, ISSN 1533-4406, 2013, Volume 369, Issue 11, pp. 1023 - 1034
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