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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
Genes & development, ISSN 0890-9369, 2013, Volume 27, Issue 10, pp. 1101 - 1114
.... Mule deficiency resulted in increased penetrance, number, and severity of skin tumors, which could be reversed by concomitant genetic knockout of c-Myc but not by knockout of p53 or p19Arf... 
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
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
Scientific reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 2487 - 12
.... QC treatment selectively upregulated cell cycle inhibitor p21, and downregulated F box protein Skp2 and p62/SQSTM1 expression independent of p53 status... 
PROGRAMMED CELL-DEATH | BREAST-CANCER | LUNG-CANCER | APOPTOSIS | SUPPRESSES TUMORIGENESIS | CARCINOMA CELLS | MULTIDISCIPLINARY SCIENCES | RESISTANCE | DEGRADATION | SKP2 | PROGRESSION | RNA, Small Interfering - genetics | Apoptosis - drug effects | Humans | Cyclin-Dependent Kinase Inhibitor p27 - agonists | Gene Expression Regulation, Neoplastic | Apoptosis - genetics | RNA, Messenger - metabolism | Autophagy - drug effects | Tumor Suppressor Protein p53 - genetics | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Ovary | Quinacrine - pharmacology | Cyclin-Dependent Kinase Inhibitor p21 - genetics | S-Phase Kinase-Associated Proteins - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Cycle Checkpoints - genetics | Female | Antineoplastic Agents - pharmacology | Autophagy - genetics | Sequestosome-1 Protein - metabolism | Signal Transduction | RNA, Messenger - genetics | Sequestosome-1 Protein - antagonists & inhibitors | Tumor Suppressor Protein p53 - metabolism | Drug Repositioning | S-Phase Kinase-Associated Proteins - metabolism | Antimalarials - pharmacology | Sequestosome-1 Protein - genetics | Cyclin-Dependent Kinase Inhibitor p21 - agonists | Cell Cycle Checkpoints - drug effects | Cell Line, Tumor | S-Phase Kinase-Associated Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p27 - genetics | RNA, Small Interfering - metabolism | Cycle protein | GTP-binding protein | Quinacrine | p53 Protein | F-box protein | mRNA | Tumor cell lines | Autophagy | Ovarian cancer | Proteins | Cyclin-dependent kinase inhibitor p21 | Cell cycle | Phagocytosis | Apoptosis
Journal Article
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
Cell death & disease, ISSN 2041-4889, 04/2019, Volume 10, Issue 4, pp. 271 - 11
.... Expression levels of cyclin-dependent kinases inhibitors (CDKIs), p21, p27, and p18 decreased during iPSC reprogramming... 
P18(INK4C) | DNA-DAMAGE | COPY NUMBER | GROWTH | CELL-CYCLE | PLURIPOTENCY | SUPPRESSION | PROTEINS | P27(KIP1) | CENTROSOME DUPLICATION | CELL BIOLOGY | Cell Division - genetics | Cyclin-Dependent Kinase Inhibitor p18 - deficiency | Transduction, Genetic | Mice, Inbred C57BL | Mice, SCID | Cyclin-Dependent Kinase Inhibitor p18 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - deficiency | Mice, Knockout | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Animals | Cyclin-Dependent Kinase Inhibitor p18 - genetics | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Chromosome Aberrations | Cyclin-Dependent Kinase 2 - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Mice, Inbred NOD | Mice | Cyclin-Dependent Kinase Inhibitor p27 - deficiency | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Cellular Reprogramming - genetics | Genomic Instability - genetics | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | Cyclin-dependent kinases | DNA damage | Stem cell transplantation | Kinases | Cyclin-dependent kinase 4 | Genomic instability | Cyclin-dependent kinase | Cyclin-dependent kinase 2 | Cyclin-dependent kinase inhibitor p21 | Clonal deletion | Efficiency | Stem cells | Cell cycle | Cyclin-dependent kinase inhibitor p27 | Pluripotency | Chromosome aberrations
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
Cell Cycle, ISSN 1551-4005, 2014, Volume 8, Issue 24, pp. 4112 - 4118
Cellular senescence is currently viewed as a response to DNA damage. In this report, we showed that non-damaging agents such as sodium butyrate-induced p21... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | DDR | DNA damage | γH2AX | Cell cycle | Cellular senescence | Aging | p21 | RAPAMYCIN | STIMULATION | cell cycle | PROTEIN-KINASE | ONCOGENE-INDUCED SENESCENCE | SUPPRESSION | CELL BIOLOGY | ARREST | cellular senescence | HISTONE H2AX PHOSPHORYLATION | gamma H2AX | QUIESCENCE | aging | ATM ACTIVATION | Cyclin-Dependent Kinase Inhibitor p21 - drug effects | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Neoplasm Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | Neoplasm Proteins - drug effects | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | DNA Damage - genetics | Neoplasm Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Biomarkers - metabolism | Cellular Senescence - genetics | Histones - ultrastructure | Stress, Physiological - genetics | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Biomarkers - analysis | Cells, Cultured | Rats | Signal Transduction - genetics | DNA - metabolism | Cell Nucleus - ultrastructure | Sirolimus - pharmacology | DNA - genetics | Animals | Histones - genetics | Cell Nucleus - genetics | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | Histones - metabolism
Journal Article