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Genes & development, ISSN 0890-9369, 2013, Volume 27, Issue 10, pp. 1101 - 1114
Tumorigenesis results from dysregulation of oncogenes and tumor suppressors that influence cellular proliferation, differentiation, apoptosis, and/or... 
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
Journal Article
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
.... The checkpoint kinases Chk1/Chk2 and the CDK inhibitor p21 are known to have important complementary roles in this process, in G2 arrest and cell cycle exit, respectively... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer | Life Sciences | Biochemistry, Molecular Biology
Journal Article
Nature communications, ISSN 2041-1723, 05/2016, Volume 7, Issue 1, p. 11363
.... Microarray analysis reveals that this combinatory inhibition significantly increases transcription and activity of cyclin-dependent kinase inhibitor p21(WAF1/CIP1... 
CELL LUNG-CANCER | SURVIVAL | COMBINATION THERAPY | STRATEGY | MULTIDISCIPLINARY SCIENCES | SYNTHETIC LETHAL INTERACTION | RESISTANCE | MUTATIONS | RAS ONCOGENES | EXPRESSION | REVEALS | Lung Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Male | Antineoplastic Agents - administration & dosage | Lung Neoplasms - physiopathology | G2 Phase - drug effects | Tumor Suppressor Protein p53 - genetics | rho-Associated Kinases - antagonists & inhibitors | Cell Cycle Proteins - antagonists & inhibitors | Enzyme Inhibitors - administration & dosage | Cyclin-Dependent Kinase Inhibitor p21 - genetics | rho-Associated Kinases - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Lung Neoplasms - genetics | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Lung Neoplasms - enzymology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | rho-Associated Kinases - genetics | Proto-Oncogene Proteins - genetics | Cell Division - drug effects | Animals | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Mice | Mice, Inbred BALB C | Mutation | Transcription | Polo-like kinase 1 | Lung cancer | Cyclin-dependent kinases | RhoA protein | Kinases | Rho-associated kinase | Cyclin-dependent kinase | Organic chemistry | Synergistic effects | Cyclin-dependent kinase inhibitor p21 | Transfection | DNA microarrays | Polo-like kinase | Rocks | Inhibition | Tumors | Cancer
Journal Article
Cell Cycle, ISSN 1551-4005, 2012, Volume 11, Issue 19, pp. 3599 - 3610
.... For this purpose, we generated a number of hTERT-immortalized senescent fibroblast cell lines overexpressing CDK inhibitors, such as p16(INK4A), p19(ARF) or p21(WAF1/CIP1... 
PD0332991 | cancer metabolism | cancer-associated fibroblast | senescence | mitophagy | autophagy | glycolysis | aging | tumor stroma | CDK inhibitors | cell cycle arrest | tumor initiation | Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Cancer-associated fibroblast | Senescence | Cancer metabolism | Tumor stroma | Aging | Cell cycle arrest | Glycolysis | Tumor initiation | Mitophagy | Autophagy | OXIDATIVE STRESS | KETONE PRODUCTION | MITOCHONDRIAL METABOLISM | STROMAL CAVEOLIN-1 | HUMAN BREAST-CANCER | CELL BIOLOGY | PREMATURE SENESCENCE | INDEPENDENT CELL-DEATH | PRIMARY BILIARY-CIRRHOSIS | AEROBIC GLYCOLYSIS | HYDROGEN-PEROXIDE | Humans | Lactic Acid - metabolism | Hydrogen Peroxide - pharmacology | Cellular Senescence - drug effects | Breast Neoplasms - blood supply | Cyclin-Dependent Kinase Inhibitor Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p19 - metabolism | Fibroblasts - pathology | Piperazines - pharmacology | Autophagy - drug effects | Neovascularization, Pathologic - pathology | Animals | Breast Neoplasms - pathology | Models, Biological | Fibroblasts - drug effects | Paracrine Communication - drug effects | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Cell Proliferation - drug effects | Mice | Pyridines - pharmacology | Cell Cycle - drug effects | Fibroblasts - metabolism | Report
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
by Chan, QKY and Lam, HM and Ng, CF and Lee, AYY and Chan, ESY and Ng, HK and Ho, SM and Lau, KM
Cell Death and Differentiation, ISSN 1350-9047, 09/2010, Volume 17, Issue 9, pp. 1511 - 1523
G-protein-coupled receptor-30 (GPR30) shows estrogen-binding affinity and mediates non-genomic signaling of estrogen to regulate cell growth. We here showed... 
COUPLED RECEPTOR GPR30 | ER-BETA | signal transduction | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | G | G-protein-coupled receptor-30 | G2/M | PROLIFERATION | G-PROTEIN | non-genomic estrogen signaling | ESTROGEN-RECEPTOR | 17-BETA-ESTRADIOL | CELL BIOLOGY | NUCLEAR ACCUMULATION | Y TRANSCRIPTION FACTOR | EXPRESSION | 1-[4-(6-bromobenzo[1,3]dioxol-5yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinolin-8-yl]-ethanone | Prostatic Neoplasms - metabolism | RNA, Small Interfering - genetics | Gene Expression - drug effects | Gene Expression - genetics | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | Receptors, G-Protein-Coupled - agonists | G2 Phase - drug effects | Quinolines - pharmacology | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Antineoplastic Agents - pharmacology | Flavonoids - pharmacology | Phosphorylation - drug effects | Prostatic Neoplasms - drug therapy | Proto-Oncogene Proteins - metabolism | Prostatic Neoplasms - pathology | Proto-Oncogene Proteins c-jun - genetics | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Proto-Oncogene Proteins c-fos - metabolism | Receptors, Estrogen - antagonists & inhibitors | Proto-Oncogene Proteins - genetics | Cyclopentanes - pharmacology | Xenograft Model Antitumor Assays | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Mice, Nude | Proto-Oncogene Proteins c-jun - metabolism | Cell Line, Tumor | Proto-Oncogene Proteins c-fos - genetics | Signal Transduction - physiology | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Receptors, G-Protein-Coupled - genetics | Cell Cycle - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 5, p. e97434
...) that are resistant to DNA damage induced apoptosis. Differentiation is associated with selective up-regulation of the Cip/Kip cyclin-dependent kinase inhibitors p57 and p21... 
STEM-CELLS | CDK INHIBITORS | CYCLE EXIT | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | MOUSE EMBRYOS | KINASE | DOWN-REGULATION | PROLIFERATION | DIFFERENTIATION | MICE LACKING | Cyclin-Dependent Kinase Inhibitor p57 - metabolism | Cell Cycle - genetics | NIH 3T3 Cells | Phosphorylation | Cell Proliferation | Cyclin-Dependent Kinase Inhibitor p57 - genetics | Humans | Apoptosis - genetics | Proto-Oncogene Proteins c-akt - genetics | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | HEK293 Cells | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Differentiation | Trophoblasts - cytology | Proto-Oncogene Proteins c-akt - metabolism | Cell Line | Trophoblasts - metabolism | Signal Transduction | Giant Cells - metabolism | Gene Expression Regulation | Giant Cells - cytology | Animals | Cytosol - metabolism | Mice | DNA Damage | Cyclin-Dependent Kinase Inhibitor p27 - genetics | DNA damage | DNA | Apoptosis | GTP-binding protein | Senescence | Childrens health | Kinases | Damage prevention | Nuclei | Proteins | Cyclin-dependent kinase | Signal transduction | Cell growth | Rodents | Cooperation | Cell cycle | Giant cells | Tumorigenesis | Cyclin-dependent kinase inhibitors | Localization | Deoxyribonucleic acid--DNA | Antigens | AKT1 protein | Cyclin-dependent kinases | Damage localization | Cyclin-dependent kinase inhibitor p21 | Monocytes | Stem cells | Cyclin-dependent kinase inhibitor p27 | Differentiation | Cytoplasm | Cancer | Deoxyribonucleic acid
Journal Article