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British Journal of Cancer, ISSN 0007-0920, 05/2009, Volume 100, Issue 9, pp. 1425 - 1433
Curcumin has been shown to inhibit the growth of various types of cancer cells; however, at concentrations much above the clinically achievable levels in... 
Curcumin | Chk1 | G2/M arrest | DNA damage | Pancreatic cancer | CARCINOMA-CELLS | DNA-DAMAGE | DOWN-REGULATION | REGULATED GENE-PRODUCTS | FACTOR-KAPPA-B | BENZYL ISOTHIOCYANATE | I CLINICAL-TRIAL | pancreatic cancer | ONCOLOGY | PROSTATE-CANCER | CHEMOPREVENTIVE AGENT | curcumin | Cell Cycle Proteins - drug effects | Protein Kinases - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Protein Kinases - genetics | Gene Silencing - drug effects | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Collagen Type XI - metabolism | DNA-Binding Proteins - metabolism | Pancreatic Neoplasms - drug therapy | Transfection | Tumor Suppressor Proteins - genetics | Caspase 3 - drug effects | Cell Cycle Proteins - genetics | Gene Expression Regulation, Neoplastic - drug effects | Protein-Serine-Threonine Kinases - metabolism | DNA Damage - drug effects | Protein Kinases - drug effects | Tumor Suppressor Proteins - metabolism | Collagen Type XI - drug effects | Pancreatic Neoplasms - pathology | Cell Cycle Proteins - metabolism | Curcumin - pharmacology | DNA-Binding Proteins - drug effects | Pancreatic Neoplasms - enzymology | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Cell Division - drug effects | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Checkpoint Kinase 1 | Tumor Suppressor Proteins - drug effects | Cell Cycle - drug effects | Translational Therapeutics | M arrest
Journal Article
Nature Medicine, ISSN 1078-8956, 07/2016, Volume 22, Issue 7, pp. 735 - 743
Immunomodulatory drugs (IMiDs), such as thalidomide and its derivatives lenalidomide and pomalidomide, are key treatment modalities for hematologic... 
MEDICINE, RESEARCH & EXPERIMENTAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | THALIDOMIDE | CEREBLON | MULTIPLE-MYELOMA CELLS | CANCER-THERAPY | CELL BIOLOGY | 5Q DELETION | LENALIDOMIDE | DEXAMETHASONE COMBINATION | MYELODYSPLASTIC SYNDROMES | T-CELLS | E3 UBIQUITIN LIGASE | Cell Cycle Proteins - drug effects | Oncogene Proteins - genetics | Peptide Hydrolases - genetics | Humans | Peptide Hydrolases - drug effects | Thalidomide - pharmacology | RNA, Messenger - metabolism | Thalidomide - analogs & derivatives | Multiple Myeloma - drug therapy | Basigin - genetics | Basigin - drug effects | Cell Cycle Proteins - genetics | Immunosuppressive Agents - pharmacology | Myelodysplastic Syndromes - drug therapy | Peptide Hydrolases - metabolism | RNA, Messenger - drug effects | Myelodysplastic Syndromes - metabolism | Teratogenesis - genetics | Cell Cycle Proteins - metabolism | Oncogene Proteins - metabolism | Multiple Myeloma - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Oncogene Proteins - drug effects | Signal Transduction - drug effects | Basigin - metabolism | Myelodysplastic Syndromes - genetics | Immunologic Factors - pharmacology | Multiple Myeloma - genetics | Teratogenesis - drug effects | Cellular proteins | Immunity | Carcinogenesis | Health aspects | Patient outcomes | Risk factors | Proteins | Drug therapy | Multiple myeloma | Tumors | Index Medicus
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 6/2006, Volume 173, Issue 5, pp. 673 - 683
In late mitosis and early G1, replication origins are licensed for subsequent use by loading complexes of the minichromosome maintenance proteins 2-7 (Mcm2-7).... 
Replication origin | Molecules | Chromatin | Spermatozoa | DNA replication | Gels | Interphase | DNA | Small interfering RNA | Ova | CYCLIN-DEPENDENT KINASES | REPLICON INITIATION | RECOGNITION COMPLEX | XENOPUS EGG EXTRACTS | PREREPLICATION COMPLEX | EUKARYOTIC DNA-REPLICATION | MINICHROMOSOME MAINTENANCE PROTEINS | ULTRAVIOLET-LIGHT | SACCHAROMYCES-CEREVISIAE | S-PHASE CHECKPOINT | CELL BIOLOGY | Cell Cycle Proteins - drug effects | Chromatin - metabolism | Hydroxyurea - pharmacology | DNA Replication - drug effects | Oxidative Stress - physiology | Adenosine Triphosphatases - drug effects | Minichromosome Maintenance Complex Component 7 | Carrier Proteins - drug effects | Minichromosome Maintenance Complex Component 2 | Minichromosome Maintenance Complex Component 3 | Minichromosome Maintenance Complex Component 4 | DNA-Binding Proteins - metabolism | Aphidicolin - pharmacology | Time Factors | Caffeine - pharmacology | Nuclear Proteins - drug effects | Chromatin - drug effects | Cell Survival - drug effects | Xenopus Proteins - drug effects | Caenorhabditis elegans - growth & development | Xenopus laevis | Cell Cycle Proteins - metabolism | DNA-Binding Proteins - drug effects | Adenosine Triphosphatases - metabolism | Nuclear Proteins - metabolism | Animals | Caenorhabditis elegans - drug effects | Carrier Proteins - metabolism | DNA Replication - physiology | Replication Origin | Xenopus Proteins - metabolism | Dormancy (Biology) | Research
Journal Article
ENDOCRINOLOGY, ISSN 0013-7227, 09/2018, Volume 159, Issue 9, pp. 3143 - 3157
Pharmacologic expansion of endogenous beta cells is a promising therapeutic strategy for diabetes. To elucidate the molecular pathways that control beta-cell... 
METABOLIC SYNDROME | PROTEIN | GLUCOSE | KINASE | MASS | EXPANSION | QUIESCENCE | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | PROLIFERATION | B-MYB | Cell Cycle Proteins - drug effects | Trans-Activators - drug effects | Humans | Middle Aged | Male | Receptor, Transforming Growth Factor-beta Type I - antagonists & inhibitors | Kv Channel-Interacting Proteins - metabolism | Transcription Factors - drug effects | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Adult | Female | Repressor Proteins - metabolism | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Kv Channel-Interacting Proteins - drug effects | NFATC Transcription Factors - metabolism | Cell Cycle Proteins - metabolism | Rats | Glycogen Synthase Kinase 3 beta - antagonists & inhibitors | Transcription Factors - metabolism | NFATC Transcription Factors - drug effects | Animals | Insulin-Secreting Cells - drug effects | Pyrazolones - pharmacology | Repressor Proteins - drug effects | Trans-Activators - metabolism | Cell Proliferation - drug effects | Forkhead Box Protein M1 - drug effects | Forkhead Box Protein M1 - metabolism | In Vitro Techniques | Cyclin-Dependent Kinase Inhibitor p27 - drug effects | Protein-Tyrosine Kinases - antagonists & inhibitors | Phosphorylation | Transcription factors | NF-AT protein | Kinases | E2F protein | Cell activation | Cell growth | Pathways | Lymphocytes | Bioactive compounds | Inhibition | Dimerization | Growth factors | Tyrosine | Glycogen | Diabetes mellitus | Glycogen synthase kinase 3 | c-Jun protein | JNK protein | Gene expression | Beta cells | Inhibitors | Cyclin-dependent kinase inhibitor p27 | Replication | Activin
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 4/2003, Volume 161, Issue 2, pp. 281 - 294
The proper segregation of sister chromatids in mitosis depends on bipolar attachment of all chromosomes to the mitotic spindle. We have identified the small... 
Mitosis | Kinetochores | Chromatids | Microtubules | HeLa cells | Cellular immunity | Chromosomes | Anaphase | Cells | Mitotic spindle apparatus | Chemical biology | Spindle assembly checkpoint | Chromosome segregation | KINASE-ACTIVITY | MAD2 | BUDDING YEAST | spindle assembly checkpoint | TENSION | G/M TRANSITION | mitosis | HISTONE H3 PHOSPHORYLATION | MAMMALIAN-CELLS | CELL BIOLOGY | kinetochores | chromosome segregation | chemical biology | VERTEBRATE SOMATIC-CELLS | Cell Cycle Proteins - drug effects | Protein Kinases - metabolism | RNA, Small Interfering - genetics | Paclitaxel - pharmacology | Humans | Nocodazole - pharmacology | Chromosome Segregation - drug effects | Mitosis - genetics | Aurora Kinase B | Microtubules - drug effects | Spindle Apparatus - genetics | Cell Cycle Proteins - genetics | Genes, cdc - physiology | Indoles - pharmacology | Kinetochores - enzymology | Protein-Serine-Threonine Kinases - metabolism | Aneugens - pharmacology | Eukaryotic Cells - enzymology | Polyploidy | Protein Kinases - drug effects | Separase | Protein-Serine-Threonine Kinases - genetics | Genes, cdc - drug effects | Aurora Kinases | Pyrimidines - pharmacology | Sulfonamides - pharmacology | Anaphase - drug effects | Phenotype | Anaphase - genetics | Animals | Eukaryotic Cells - drug effects | Mitosis - drug effects | Microtubules - genetics | Microtubules - enzymology | Protein-Serine-Threonine Kinases - drug effects | Eukaryotic Cells - cytology | Kinetochores - drug effects | Spindle Apparatus - drug effects | HeLa Cells | Thiones - pharmacology | Endopeptidases | Chromosome Segregation - genetics | Spindle Apparatus - enzymology | Research | mitosis; chromosome segregation; kinetochores; spindle assembly checkpoint; chemical biology
Journal Article
The FASEB journal : official publication of the Federation of American Societies for Experimental Biology, ISSN 0892-6638, 2001, Volume 15, Issue 14, pp. 2742 - 2744
The regular use of various nonsteroidal anti-inflammatory drugs (NSAIDs) was shown to decrease the incidence of colorectal cancer. This effect is thought to be... 
KINASE-ACTIVITY | BIOCHEMISTRY & MOLECULAR BIOLOGY | cyclooxygenase | MAMMALIAN-CELLS | SULINDAC SULFONE | SC560 | CELL BIOLOGY | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | NSAIDs | COLORECTAL-CANCER | PROSTATE-CANCER | BIOLOGY | FAMILIAL ADENOMATOUS POLYPOSIS | IONIZING-RADIATION | G/G-phase block | R-FLURBIPROFEN | CYCLOOXYGENASE-2 INHIBITOR | Cell Cycle Proteins - drug effects | Apoptosis - drug effects | Colonic Neoplasms - drug therapy | Cyclooxygenase 2 | Humans | Colonic Neoplasms - metabolism | Dose-Response Relationship, Drug | Cyclins - metabolism | Cyclins - drug effects | Isoenzymes - metabolism | Tumor Cells, Cultured | Pyrazoles - pharmacology | Caco-2 Cells | Cell Survival - drug effects | Tumor Suppressor Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 | Cell Cycle Proteins - metabolism | Celecoxib | Sulfonamides - pharmacology | Blotting, Western | Cell Division - drug effects | Cyclin-Dependent Kinase Inhibitor p27 | Cyclooxygenase Inhibitors - pharmacology | HT29 Cells | Membrane Proteins | Xenograft Model Antitumor Assays | Animals | Cyclooxygenase 2 Inhibitors | Mice, Nude | Prostaglandin-Endoperoxide Synthases - metabolism | Colonic Neoplasms - pathology | Cell Cycle - physiology | Mice | Tumor Suppressor Proteins - drug effects | Cell Cycle - drug effects | Isoenzymes - antagonists & inhibitors
Journal Article
Journal of Neuro-Oncology, ISSN 0167-594X, 12/2007, Volume 85, Issue 3, pp. 263 - 270
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 08/2007, Volume 102, Issue 3, pp. 667 - 678
Microglial cells release monocyte chemoattractant protein‐1 (MCP‐1) which amplifies the inflammation process by promoting recruitment of macrophages and... 
mitogen‐activated protein kinase phosphatase‐1 | monocyte chemoattractant protein‐1 | p38 | neuroinflammation | glucocorticoids | microglia | Jun N‐terminal kinase | Monocyte chemoattractant protein-1 | Mitogen-activated protein kinase phosphatase-1 | Glucocorticoids | Neuroinflammation | Jun N-terminal kinase | Microglia | mitogen-activated protein kinase phosphatase-1 | jun N-terminal kinase | MAP KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | monocyte chemoattractant protein-1 | CHEMOTACTIC PROTEIN-1 | KAPPA-B | GLIAL-CELLS | NEUROSCIENCES | INDUCED EXPRESSION | MULTIPLE-SCLEROSIS | STIMULATED MACROPHAGES | CENTRAL-NERVOUS-SYSTEM | CHEMOKINE RECEPTORS | PROINFLAMMATORY CYTOKINE BIOSYNTHESIS | Cell Cycle Proteins - drug effects | Dual Specificity Phosphatase 1 | Rats, Wistar | Coculture Techniques | Phosphoprotein Phosphatases - metabolism | JNK Mitogen-Activated Protein Kinases - metabolism | Protein Tyrosine Phosphatases - metabolism | Immediate-Early Proteins - drug effects | Protein Tyrosine Phosphatases - drug effects | MAP Kinase Signaling System - immunology | Cell Movement - immunology | Immediate-Early Proteins - metabolism | Dexamethasone - pharmacology | Encephalitis - physiopathology | Microglia - immunology | Phosphoprotein Phosphatases - drug effects | Encephalitis - drug therapy | Chemokine CCL2 - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Chemotaxis - immunology | Protein Phosphatase 1 | Microglia - drug effects | Anti-Inflammatory Agents - pharmacology | Brain - physiopathology | Cell Cycle Proteins - metabolism | Cells, Cultured | Microglia - enzymology | Rats | Encephalitis - immunology | Treatment Outcome | Chemotaxis - drug effects | Down-Regulation - drug effects | Brain - drug effects | Down-Regulation - physiology | Cell Movement - drug effects | Animals | MAP Kinase Signaling System - drug effects | Chemokine CCL2 - antagonists & inhibitors | Brain - immunology | Protein kinases | Esterases | Dexamethasone | Neurosciences | Cellular biology | Molecular biology | Gene expression | Kinases | Inflammatory diseases | Cell adhesion & migration
Journal Article
Biomedicine & Pharmacotherapy, ISSN 0753-3322, 2010, Volume 64, Issue 10, pp. 733 - 740
Abstract HDACs and HATs regulate histone acetylation, an epigenetic modification that controls chromatin structure and through it, gene expression. Butyrate, a... 
Internal Medicine | Medical Education | Histone modifications | Vascular smooth muscle cells | Butyrate | MEDICINE, RESEARCH & EXPERIMENTAL | MECHANISM | PROLIFERATION | COLON-CANCER | EPITHELIAL-CELLS | SODIUM-BUTYRATE | DEACETYLASE INHIBITORS | BIOLOGY | GENE-EXPRESSION | CARDIOVASCULAR-DISEASE | PHARMACOLOGY & PHARMACY | HUNTINGTONS-DISEASE | Cell Cycle Proteins - drug effects | Chromatin - metabolism | Cyclin-Dependent Kinases - metabolism | Muscle, Smooth, Vascular - metabolism | Atherosclerosis - genetics | Butyrates - pharmacology | Transcriptional Activation - drug effects | Cyclins - genetics | G1 Phase - drug effects | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cyclins - metabolism | Protein Processing, Post-Translational - drug effects | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cyclin-Dependent Kinases - antagonists & inhibitors | Phosphorylation - drug effects | Cyclin-Dependent Kinases - genetics | Muscle, Smooth, Vascular - drug effects | Retinoblastoma Protein - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Rats | Down-Regulation - drug effects | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Acetylation - drug effects | Animals | Histones - genetics | Mitosis - drug effects | Methylation - drug effects | Retinoblastoma Protein - antagonists & inhibitors | Histone Deacetylase Inhibitors - pharmacology | Cell Proliferation - drug effects | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Histones - metabolism | Cell Cycle - drug effects | Esters | Chromatin | Gene expression | Analysis |