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Blood, ISSN 0006-4971, 09/2015, Volume 126, Issue 11, pp. 1273 - 1280
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 8, p. e12304
Gliomas are morbid brain tumors that are extremely resistant to available chemotherapy and radiology treatments. Some studies have suggested that... 
BREAST-CANCER CELLS | BRAIN-TUMOR | INHIBITION | MULTIDISCIPLINARY SCIENCES | CA2+-ACTIVATED K+ CHANNELS | GROWTH | CLOTRIMAZOLE | INTERMEDIATE-CONDUCTANCE | EPIDEMIOLOGY | MODULATION | CYCLE | Potassium - metabolism | RNA, Small Interfering - genetics | Large-Conductance Calcium-Activated Potassium Channels - metabolism | Small-Conductance Calcium-Activated Potassium Channels - genetics | Intermediate-Conductance Calcium-Activated Potassium Channels - genetics | Humans | Large-Conductance Calcium-Activated Potassium Channels - deficiency | Molecular Sequence Data | Electric Conductivity | Large-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | RNA, Messenger - metabolism | Gene Knockdown Techniques | Glioblastoma - genetics | Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | Large-Conductance Calcium-Activated Potassium Channels - genetics | Gene Expression Regulation, Neoplastic - drug effects | Potassium Channel Blockers - pharmacology | Amino Acid Sequence | RNA, Messenger - genetics | Down-Regulation - genetics | Glioblastoma - surgery | Glioblastoma - pathology | Intermediate-Conductance Calcium-Activated Potassium Channels - deficiency | Cell Line, Tumor | Cell Proliferation - drug effects | Chemotherapy | Gliomas | Genes | Brain tumors | Genetic engineering | Potassium channels | Cancer | Cell proliferation | Brain | Biotechnology | Neurosciences | Calcium | Brain cancer | Glioblastoma | Smooth muscle | Potassium conductance | Kinases | Cancer therapies | Channels | Potassium channels (calcium-gated) | Proteins | Cell growth | Surgery | Glioma cells | Cell cycle | Physiology | Calcium channels | Channel gating | Tumor cells | siRNA | Pharmacology | Glioblastoma multiforme | Resistance | Studies | Polymerase chain reaction | Gene silencing | Inhibitors | Radiology | Conductance | Glioblastoma cells | Potassium | Prostate cancer | Clotrimazole | Tumors | Cultures
Journal Article
Cellular Physiology and Biochemistry, ISSN 1015-8987, 04/2018, Volume 46, Issue 2, pp. 765 - 780
Background/Aims: Based on the protective effect of crocin against cardiovascular diseases, we hypothesize that crocin could improve endothelial function... 
Original Paper | Endothelial nitric oxide synthase | Endothelial function | Intermediate-conductance Ca | Activated K+ channels | Crocin | conductance Ca2+ activated K+ channels | OXIDATIVE STRESS | PHYSIOLOGY | SUBCHRONIC EXPOSURE | CELL BIOLOGY | BREAST-CANCER CELLS | K-CA-CHANNELS | INDUCED CARDIOTOXICITY | Intermediate | HYPERPOLARIZING FACTOR | CORPUS CAVERNOSUM | NITRIC-OXIDE | INFLAMMATORY RESPONSE | HYPERTENSIVE-RATS | Human Umbilical Vein Endothelial Cells | Intermediate-Conductance Calcium-Activated Potassium Channels - genetics | Calcium - metabolism | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Aorta - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | Carotenoids - pharmacology | Thrombomodulin - metabolism | RNA Interference | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | Flavonoids - pharmacology | Nitric Oxide Synthase Type III - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Pyrazoles - pharmacology | Aorta - drug effects | Rats | Down-Regulation - drug effects | Rats, Sprague-Dawley | Aorta - pathology | Cell Movement - drug effects | Intercellular Adhesion Molecule-1 - metabolism | Animals | Signal Transduction - drug effects | Cell Proliferation - drug effects | Nitric Oxide - metabolism | Vascular Cell Adhesion Molecule-1 - metabolism | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | RNA, Small Interfering - metabolism | Cell growth | Nitric oxide | Rodents | Cell adhesion & migration | Intermediate-conductance Ca2+-activated K+ channels
Journal Article
by Wang, LP and Wang, Y and Zhao, LM and Li, GR and Deng, XL
BIOCHEMICAL PHARMACOLOGY, ISSN 0006-2952, 05/2013, Volume 85, Issue 10, pp. 1486 - 1494
The proliferation of cardiac fibroblasts is implicated in the pathogenesis of myocardial remodeling and fibrosis. Intermediate-conductance calcium-activated K+... 
CONDUCTANCE | MIGRATION | PROTEIN-KINASE-C | Intermediate-conductance Ca2+ activated | CA2+-ACTIVATED K+ CHANNELS | Proliferation | MESENCHYMAL STEM-CELLS | CALCIUM | K+ channels | Cardiac fibroblasts | PHARMACOLOGY & PHARMACY | SMOOTH-MUSCLE-CELLS | ACTIVATED POTASSIUM CHANNEL | ION CHANNELS | Angiotensin II | EXPRESSION | Heart Ventricles - cytology | Intermediate-Conductance Calcium-Activated Potassium Channels - genetics | Transcription Factor AP-1 - genetics | Male | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | Angiotensin II Type 1 Receptor Blockers - pharmacology | Transcription Factor AP-1 - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels - agonists | Receptor, Angiotensin, Type 1 - genetics | Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | Fibroblasts - metabolism | Pyrazoles - pharmacology | Vasoconstrictor Agents - pharmacology | Angiotensin II - pharmacology | Losartan - pharmacology | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Rats, Sprague-Dawley | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Patch-Clamp Techniques | Transcription Factor AP-1 - antagonists & inhibitors | Animals | Signal Transduction - drug effects | Fibroblasts - drug effects | Receptor, Angiotensin, Type 1 - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Proliferation - drug effects | Fibroblasts - cytology | Heart Ventricles - metabolism | Protein Kinase Inhibitors - pharmacology | Primary Cell Culture | Heart Ventricles - drug effects
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2010, Volume 107, Issue 4, pp. 1541 - 1546
The calcium-activated K⁺ channel KCa3.1 plays an important role in T lymphocyte Ca²⁺ signaling by helping to maintain a negative membrane potential, which... 
Beta cells | Crohn disease | Inflammatory bowel diseases | Cytokines | Spleen cells | Lymphocytes | Memory | Antibodies | Mice | Colitis | Calcium signaling | Inflammatory bowel disease | T helper cells | Potassium channels | T-cell signaling | CROHNS-DISEASE | AUTOIMMUNE INFLAMMATION | PHYSIOLOGICAL ROLES | MULTIDISCIPLINARY SCIENCES | calcium signaling | ULCERATIVE-COLITIS | inflammatory bowel disease | INTESTINAL INFLAMMATION | GROWTH-FACTOR-BETA | INFLAMMATORY-BOWEL-DISEASE | KV1.3 CHANNELS | potassium channels | ACTIVATED POTASSIUM CHANNEL | INTERMEDIATE-CONDUCTANCE | Intermediate-Conductance Calcium-Activated Potassium Channels - immunology | Colitis - genetics | Colitis - pathology | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | DNA-Binding Proteins - deficiency | CD4-Positive T-Lymphocytes - immunology | T-Lymphocytes, Helper-Inducer - immunology | T-Lymphocytes, Helper-Inducer - cytology | Receptors, Antigen, T-Cell - immunology | Cell Differentiation | Colitis - immunology | Cytokines - immunology | Disease Models, Animal | B-Lymphocytes - cytology | DNA-Binding Proteins - immunology | T-Lymphocytes, Helper-Inducer - metabolism | CD4-Positive T-Lymphocytes - cytology | Mice, Inbred C57BL | CD4-Positive T-Lymphocytes - metabolism | Cells, Cultured | Mice, Knockout | Animals | B-Lymphocytes - immunology | Intermediate-Conductance Calcium-Activated Potassium Channels - deficiency | Colitis - metabolism | Cytokines - biosynthesis | Biological Sciences
Journal Article
Scientific Reports, ISSN 2045-2322, 03/2016, Volume 6, Issue 1, p. 23884
Autophagy is emerging as an important pathway in many diseases including diabetic nephropathy. It is acknowledged that oxidative stress plays a critical role... 
OXIDATIVE STRESS | EMERGING ROLE | MULTIDISCIPLINARY SCIENCES | THERAPEUTIC TARGET | DISEASE | INJURY | MICE | INTERMEDIATE-CONDUCTANCE | UP-REGULATION | NEPHROPATHY | POTASSIUM CHANNEL | RNA, Small Interfering - genetics | Epithelial Cells - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels - genetics | TOR Serine-Threonine Kinases - metabolism | Streptozocin | Epithelial Cells - drug effects | Humans | Diabetes Mellitus, Experimental - genetics | Male | Phosphatidylinositol 3-Kinases - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | Proto-Oncogene Proteins c-akt - genetics | TOR Serine-Threonine Kinases - genetics | Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors | Diabetes Mellitus, Experimental - chemically induced | Autophagy - genetics | Diabetes Mellitus, Experimental - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Transforming Growth Factor beta1 - pharmacology | Diabetic Nephropathies - pathology | Kidney Tubules, Proximal - pathology | Signal Transduction | Diabetic Nephropathies - metabolism | Phagosomes - metabolism | Diabetic Nephropathies - chemically induced | Gene Expression Regulation | Diabetic Nephropathies - genetics | Epithelial Cells - pathology | Mice, Knockout | Phosphatidylinositol 3-Kinases - genetics | Animals | Kidney Tubules, Proximal - metabolism | Diabetes Mellitus, Experimental - pathology | Mice | Cell Line, Transformed | RNA, Small Interfering - metabolism | TOR protein | Oxidative stress | Phosphorylation | Kidneys | Diabetes mellitus | AKT protein | siRNA | Autophagy | 1-Phosphatidylinositol 3-kinase | Signal transduction | Nephropathy | Rodents | Fibrosis | Nitrotyrosine | Diabetes | Vacuoles | Phagocytosis | Kidney transplantation
Journal Article
British Journal of Pharmacology, ISSN 0007-1188, 01/2012, Volume 165, Issue 1, pp. 223 - 234
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2008, Volume 105, Issue 28, pp. 9627 - 9632
Journal Article
Neuropharmacology, ISSN 0028-3908, 10/2017, Volume 125, pp. 386 - 395
Journal Article
Cell Death and Disease, ISSN 2041-4889, 08/2013, Volume 4, Issue 8, pp. e773 - e773
Glioblastoma multiforme (GBM) is a diffuse brain tumor characterized by high infiltration in the brain parenchyma rendering the tumor difficult to eradicate by... 
dependent K | channels | Astrocytes | Invasion | Glioblastoma | Microglia | MIGRATION | OPERATOR-REPRESSOR SYSTEM | CELLS | CA2+-ACTIVATED K+ CHANNEL | TUMOR GRADE | Ca2+-dependent K+ channels | CELL BIOLOGY | glioblastoma | invasion | GROWTH | MALIGNANT GLIOMAS | ACTIVATED POTASSIUM CHANNEL | astrocytes | ION CHANNELS | microglia | EXPRESSION | Gene Silencing - drug effects | Neuroglia - pathology | Humans | Astrocytes - pathology | Brain Neoplasms - pathology | Male | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | Brain Neoplasms - metabolism | Neuroglia - drug effects | Brain - metabolism | Glioblastoma - metabolism | Potassium Channel Blockers - pharmacology | Pyrazoles - pharmacology | Astrocytes - drug effects | Neoplasm Invasiveness | Mice, Inbred C57BL | Mice, SCID | Brain - drug effects | Xenograft Model Antitumor Assays | Cell Movement - drug effects | Animals | Glioblastoma - pathology | Brain - pathology | Cell Line, Tumor | Neuroglia - metabolism | Mice | Astrocytes - metabolism | RNA, Small Interfering - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels | Brain | Pyrazoles | Neuroglia | Neurons and Cognition | Gene Silencing | Brain Neoplasms | Life Sciences | RNA, Small Interfering | Potassium Channel Blockers | Cell Movement | Original | Ca2+-dependent K+channels
Journal Article