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The Journal of immunology (1950), ISSN 1550-6606, 2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors
Journal Article
Nature (London), ISSN 1476-4687, 2015, Volume 526, Issue 7571, pp. 136 - 139
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2009, Volume 119, Issue 12, pp. 3626 - 3636
The polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) is dysregulated in various cancers, and its upregulation strongly correlates... 
MEDICINE, RESEARCH & EXPERIMENTAL | BREAST-CANCER CELLS | DEVELOPMENTAL REGULATORS | CELLULAR MEMORY | E-CADHERIN EXPRESSION | HEMATOPOIETIC STEM-CELLS | PROSTATE-CANCER | MYC TRANSGENIC MICE | SELF-RENEWAL | NF-KAPPA-B | TRANSCRIPTION FACTOR | Nasopharyngeal Neoplasms - genetics | Neoplasm Transplantation | Nasopharyngeal Neoplasms - metabolism | Epithelial Cells - metabolism | Cadherins - metabolism | Humans | Glycogen Synthase Kinase 3 beta | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Mesoderm - cytology | Repressor Proteins - antagonists & inhibitors | Nasopharyngeal Neoplasms - pathology | Cadherins - genetics | Epithelial Cells - cytology | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Nasopharyngeal Neoplasms - etiology | Snail Family Transcription Factors | Nasopharynx - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | PTEN Phosphohydrolase - genetics | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Neoplasm Invasiveness | Down-Regulation | Gene Silencing | PTEN Phosphohydrolase - metabolism | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Animals | Polycomb Repressive Complex 1 | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mesoderm - metabolism | Mice | Nasopharynx - cytology | Chromatin | Care and treatment | Lymphomas | Research | Analysis | Cancer
Journal Article
The EMBO Journal, ISSN 0261-4189, 2011, Volume 30, Issue 4, pp. 770 - 782
Notch signalling is important for development and tissue homeostasis and activated in many human cancers. Nevertheless, mutations in Notch pathway components... 
miR‐200 | ZEB1 | EMT | Notch | stemness | miR-200 | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | PHENOTYPE | E-CADHERIN | MIR-200 FAMILY | REPRESSORS ZEB1 | CELL BIOLOGY | EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | COLORECTAL-CANCER | Receptors, Notch - metabolism | Humans | Receptors, Notch - genetics | Gene Knockdown Techniques | Intercellular Signaling Peptides and Proteins - physiology | DNA-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Neoplasms - genetics | Membrane Proteins - physiology | Serrate-Jagged Proteins | Base Sequence | Membrane Proteins - metabolism | Nuclear Proteins - genetics | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Transcription Factors - physiology | DNA-Binding Proteins - antagonists & inhibitors | Membrane Proteins - genetics | Cells, Cultured | Intercellular Signaling Peptides and Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Signal Transduction - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Models, Biological | Calcium-Binding Proteins - physiology | Homeodomain Proteins - antagonists & inhibitors | Nuclear Proteins - antagonists & inhibitors | Signal Transduction - physiology | MicroRNAs - genetics | Feedback, Physiological - physiology | MicroRNAs - physiology | Homeodomain Proteins - physiology | Calcium-Binding Proteins - genetics | Zinc Finger E-box-Binding Homeobox 1 | Proteins | Signal transduction | Cellular biology | Molecular biology | Gene expression | Cancer
Journal Article
Nature (London), ISSN 1476-4687, 2012, Volume 483, Issue 7391, pp. 598 - 602
...). Whereas several proteins are known to regulate chromatin marks associated with the distinct epigenetic states of cells before and after reprogramming(2,3... 
CELLS | LEUKEMIA | PRC2 | HISTONE METHYLATION | MULTIDISCIPLINARY SCIENCES | PLURIPOTENT | Chromatin - metabolism | Homeodomain Proteins - metabolism | Humans | Methyltransferases - metabolism | Methyltransferases - genetics | Methyltransferases - biosynthesis | YY1 Transcription Factor - metabolism | Repressor Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Kruppel-Like Transcription Factors - metabolism | YY1 Transcription Factor - antagonists & inhibitors | Induced Pluripotent Stem Cells - cytology | Cellular Reprogramming - genetics | Repressor Proteins - metabolism | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Nanog Homeobox Protein | Transcription Factors - antagonists & inhibitors | DNA Methylation - genetics | Polycomb-Group Proteins | Proto-Oncogene Proteins c-myc - metabolism | Enhancer of Zeste Homolog 2 Protein | Transcription Factors - metabolism | Polycomb Repressive Complex 2 | Methyltransferases - antagonists & inhibitors | Fibroblasts - cytology | RNA, Small Interfering | Histones - metabolism | Methylation | Chromatin - genetics | RNA-Binding Proteins - metabolism | Physiological aspects | Chromatin | Genetic aspects | Research | Methyltransferases | Embryonic stem cells | Enzymes | Efficiency | Stem cells | Epigenetics | Kinases | Gene expression | Apoptosis
Journal Article
Cell death & disease, ISSN 2041-4889, 2012, Volume 3, Issue 10, pp. e398 - e398
Glioblastoma multiforme (GBM) is a heterogeneous disease despite its seemingly uniform pathology. Deconvolution of The Cancer Genome Atlas's GBM gene... 
microRNA-10b | Angiogenicity | Invasion | Glioblastoma | Apoptosis | GLIOMA-CELLS | SUPPRESSOR | ACTIVATION | ANGIOGENESIS | angiogenicity | THROMBOSPONDIN-1 | apoptosis | P53 | CELL BIOLOGY | CYLD | glioblastoma | invasion | GENE-EXPRESSION | NF-KAPPA-B | ENDOTHELIAL GROWTH-FACTOR | Paired Box Transcription Factors - genetics | MicroRNAs - antagonists & inhibitors | Tumor Suppressor Protein p53 - antagonists & inhibitors | Homeodomain Proteins - metabolism | Humans | Neovascularization, Pathologic | Baculoviridae - genetics | MicroRNAs - metabolism | Transplantation, Heterologous | Repressor Proteins - antagonists & inhibitors | Tumor Suppressor Protein p53 - genetics | Glioblastoma - genetics | RNA Interference | Glioblastoma - metabolism | Eye Proteins - antagonists & inhibitors | Eye Proteins - genetics | Repressor Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Genetic Vectors - metabolism | Repressor Proteins - genetics | Transcription Factors - antagonists & inhibitors | PAX6 Transcription Factor | Paired Box Transcription Factors - antagonists & inhibitors | Receptor, Notch1 - metabolism | Transcription Factors - genetics | Genetic Vectors - genetics | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Animals | Eye Proteins - metabolism | Glioblastoma - pathology | Homeodomain Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Receptor, Notch1 - antagonists & inhibitors | Receptor, Notch1 - genetics | Paired Box Transcription Factors - metabolism | Cell Movement | RNA, Small Interfering - metabolism | Original
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2016, Volume 113, Issue 50, pp. E8051 - E8058
Protein−protein interactions play a central role in cellular function. Improving the understanding of complex formation has many practical applications... 
Druggable surface | Direct coupling analysis | Drug design | Protein-protein interface | Hot spots | drug design | MULTIDISCIPLINARY SCIENCES | DRUG DISCOVERY | DIMERIZATION | protein-protein interface | INHIBITION | CONSERVATION | hot spots | CDK1 | HOT-SPOTS | direct coupling analysis | HIV-1 PROTEASE | BINDING-SITES | WEB SERVER | druggable surface | COMPUTATIONAL PREDICTION | Histone Deacetylase 1 - chemistry | Molecular Probes | HIV Protease - drug effects | Humans | Proto-Oncogene Proteins c-mdm2 - chemistry | CDC2-CDC28 Kinases - antagonists & inhibitors | Repressor Proteins - antagonists & inhibitors | HIV Protease Inhibitors - pharmacology | Proto-Oncogene Proteins c-mdm2 - drug effects | CDC2 Protein Kinase - drug effects | Drug Design | Histone Deacetylase 1 - drug effects | CDC2 Protein Kinase - chemistry | Histone Deacetylase 1 - antagonists & inhibitors | Binding Sites | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Molecular Docking Simulation - methods | Repressor Proteins - chemistry | Protein Interaction Domains and Motifs - drug effects | CDC2 Protein Kinase - antagonists & inhibitors | HIV-1 - drug effects | CDC2-CDC28 Kinases - chemistry | CDC2-CDC28 Kinases - drug effects | Histone Deacetylases - chemistry | HIV Protease Inhibitors - chemistry | Tumor Necrosis Factor-alpha - chemistry | Tumor Necrosis Factor-alpha - drug effects | HIV-1 - enzymology | Histone Deacetylases - drug effects | Repressor Proteins - drug effects | HIV Protease - chemistry | Protein Multimerization - drug effects | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Evolution, Molecular | Observations | Protein-protein interactions | Biological Sciences | PNAS Plus | protein−protein interface
Journal Article
Scientific reports, ISSN 2045-2322, 2016, Volume 6, Issue 1, p. 21810
Protein arginine methyltransferase 1 (PRMT1) catalyzes methylation of histones and other cellular proteins, and thus regulates gene transcription and protein activity... 
PROTEIN METHYLATION | ARGININE METHYLTRANSFERASE 1 | INHIBITION | ACTIVATOR | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | GROWTH-FACTOR | KAPPA-B | SIGNAL TRANSDUCER | Interleukin-1beta - pharmacology | Humans | Phosphatidylethanolamine Binding Protein - metabolism | NF-kappa B - metabolism | Protein Inhibitors of Activated STAT - metabolism | STAT6 Transcription Factor - genetics | Vascular Endothelial Growth Factor A - metabolism | Interleukin-1beta - genetics | Recombinant Proteins - biosynthesis | RNA, Messenger - metabolism | Vascular Endothelial Growth Factor A - genetics | Repressor Proteins - antagonists & inhibitors | Interleukin-4 - pharmacology | RNA Interference | Cyclooxygenase 2 - genetics | Interleukin-1beta - metabolism | Protein Inhibitors of Activated STAT - genetics | STAT6 Transcription Factor - antagonists & inhibitors | Phosphorylation - drug effects | Binding Sites | Real-Time Polymerase Chain Reaction | Repressor Proteins - metabolism | Fibroblasts - metabolism | Phosphatidylethanolamine Binding Protein - antagonists & inhibitors | A549 Cells | NF-kappa B - antagonists & inhibitors | Repressor Proteins - genetics | STAT6 Transcription Factor - metabolism | Blotting, Western | Small Ubiquitin-Related Modifier Proteins - antagonists & inhibitors | Signal Transduction - drug effects | Fibroblasts - cytology | Pneumonia - metabolism | RNA, Small Interfering - metabolism | Epithelial Cells - metabolism | Immunoprecipitation | Pneumonia - pathology | Protein-Arginine N-Methyltransferases - antagonists & inhibitors | Recombinant Proteins - isolation & purification | Small Ubiquitin-Related Modifier Proteins - genetics | Lung - metabolism | Protein-Arginine N-Methyltransferases - genetics | Interleukin-4 - genetics | Epithelial Cells - cytology | Protein Inhibitors of Activated STAT - antagonists & inhibitors | Promoter Regions, Genetic | Lung - pathology | Small Ubiquitin-Related Modifier Proteins - metabolism | Interleukin-4 - metabolism | Cells, Cultured | Recombinant Proteins - pharmacology | Protein-Arginine N-Methyltransferases - metabolism | Up-Regulation - drug effects | Phosphatidylethanolamine Binding Protein - genetics | Cyclooxygenase 2 - metabolism | Microscopy, Fluorescence | Immunohistochemistry | NF-κB protein | Transcription | Epithelial cells | Protein arginine methyltransferase | Epithelium | Kinases | Western blotting | Asthma | Proteins | Signal transduction | Interleukin 4 | Arginine | Stat6 protein | Fibroblasts | Histones | DNA methylation
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2007, Volume 117, Issue 12, pp. 3765 - 3773
S-phase kinase-associated protein 2 (SKP2) is a component of the E3 ubiquitin ligase SKP1-Cul1-Fbox complex... 
MEDICINE, RESEARCH & EXPERIMENTAL | UBIQUITIN-MEDIATED DEGRADATION | BOX PROTEIN SKP2 | ENTEROPATHY | DISRUPTION | P27 | MOUSE | SCURFY | EXPRESSION | CELL-CYCLE INHIBITION | P27(KIP1) | Oncogene Proteins - genetics | RNA, Small Interfering - genetics | Receptor, ErbB-2 - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Receptor, ErbB-2 - metabolism | Repressor Proteins - antagonists & inhibitors | Breast Neoplasms - metabolism | Genes, X-Linked | S-Phase Kinase-Associated Proteins - antagonists & inhibitors | Cell Transformation, Neoplastic - genetics | Forkhead Transcription Factors - metabolism | Mice, Mutant Strains | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Cullin Proteins - metabolism | Female | Forkhead Transcription Factors - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Gene Expression Regulation, Neoplastic - genetics | Repressor Proteins - metabolism | Tumor Suppressor Proteins - metabolism | RNA, Small Interfering - pharmacology | Cell Cycle Proteins - metabolism | Gene Silencing | Oncogene Proteins - metabolism | Repressor Proteins - genetics | Forkhead Transcription Factors - genetics | S-Phase Kinase-Associated Proteins - metabolism | Cell Transformation, Neoplastic - metabolism | Oncogene Proteins - antagonists & inhibitors | Cullin Proteins - genetics | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Ploidies | Cell Line, Tumor | Heterozygote | S-Phase Kinase-Associated Proteins - genetics | Mice | Mice, Inbred BALB C | Cell Transformation, Neoplastic - pathology | Tumor suppressor genes | Breast cancer | Genetic aspects | Research | DNA binding proteins | Identification and classification | Health aspects | Risk factors
Journal Article
PloS one, ISSN 1932-6203, 2019, Volume 14, Issue 2, p. e0211980
... (Shh) signaling pathway and its downstream transcription factors gli are considered as one of these mechanisms [1-3]. The gli1, gli2 and gli3 proteins are required... 
PROTEIN-KINASE-A | STEM-CELLS | GLIOBLASTOMA | MESSENGER-RNA | CELL SELF-RENEWAL | SIGNALING PATHWAY | SPLICE VARIANT | MULTIDISCIPLINARY SCIENCES | KRUPPEL FAMILY | EXPRESSION | SONIC-HEDGEHOG | Neoplastic Stem Cells - drug effects | Humans | Brain Neoplasms - metabolism | Repressor Proteins - antagonists & inhibitors | Gene Knockdown Techniques | Glioma - metabolism | Glioma - genetics | Neoplastic Stem Cells - metabolism | Zinc Finger Protein Gli2 - antagonists & inhibitors | Zinc Finger Protein GLI1 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Nuclear Proteins - genetics | Zinc Finger Protein Gli2 - genetics | Cell Survival - drug effects | Nerve Tissue Proteins - antagonists & inhibitors | Zinc Finger Protein GLI1 - genetics | Zinc Finger Protein Gli3 - antagonists & inhibitors | Brain Neoplasms - genetics | Repressor Proteins - genetics | Pyrimidines - pharmacology | Nerve Tissue Proteins - genetics | Zinc Finger Protein Gli3 - genetics | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Forkhead Box Protein M1 - genetics | Pyridines - pharmacology | HeLa Cells | Research | DNA binding proteins | Gene expression | Gliomas | Cell death | Stem cells | Brain | Biotechnology | Transformation | Transcription factors | Dehydrogenases | Brain cancer | Genes | Oct-4 protein | Differentiation (biology) | Kinases | Tissues | Cell adhesion & migration | Proteins | Demethylation | Signal transduction | Embryogenesis | Glioma cells | Cell cycle | Deoxyribonucleic acid--DNA | Cell survival | siRNA | Cell differentiation | Survival | Embryonic growth stage | Brain research | Cell lines | Ligands | Nuclear physics | Deoxyribonucleic acid | DNA
Journal Article