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Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2008, Volume 121, Issue 4, pp. 893 - 902.e2
.... Objectives We sought to study the activation of the mitogen-activated protein kinase (MAPK) signaling pathway in airway cells... 
Allergy and Immunology | mitogen-activated protein kinase | chemokines | epithelial function | bronchial biopsy | Asthma | LUNG | BRONCHIAL EPITHELIAL-CELLS | MAP KINASE | asthma | PROLIFERATION | IMMUNOLOGY | ALLERGY | GM-CSF | PATHWAY | INFLAMMATION | SMOOTH-MUSCLE-CELLS | DIFFERENTIATION | EXPRESSION | Phosphorylation | Bronchi - enzymology | Humans | Middle Aged | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Enzyme Induction - immunology | MAP Kinase Signaling System - immunology | Enzyme Activation - immunology | Respiratory Mucosa - pathology | Chemokines - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - biosynthesis | Adult | Female | p38 Mitogen-Activated Protein Kinases - metabolism | Bronchi - pathology | Respiratory Mucosa - secretion | Chemokines - biosynthesis | Chemokines - secretion | Mitogen-Activated Protein Kinase 1 - physiology | p38 Mitogen-Activated Protein Kinases - physiology | Asthma - enzymology | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Respiratory Mucosa - enzymology | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - physiology | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Asthma - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Protein kinases | Proteins | Studies | Signal transduction | Cell culture | Rodents | Cloning | Smooth muscle | Kinases
Journal Article
Scientific reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 1480 - 11
.... In normal retinas, intravitreal injection of BaCl2 significantly increased GFAP expression in Muller cells, which was eliminated by co-injecting mitogen-activated protein kinase (MAPK) inhibitor U0126... 
ACTIVATED PROTEIN-KINASE | MESSENGER-RNA | POTASSIUM CHANNELS | MULTIDISCIPLINARY SCIENCES | GANGLION-CELLS | MEMBRANE CONDUCTANCE | INTRAOCULAR-PRESSURE | OCULAR HYPERTENSION MODEL | GLIAL-CELLS | EXPERIMENTAL GLAUCOMA | NUCLEUS-ACCUMBENS | Retina - drug effects | Glial Fibrillary Acidic Protein - genetics | Retina - metabolism | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Ependymoglial Cells - metabolism | Gliosis - chemically induced | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Ocular Hypertension - metabolism | Glial Fibrillary Acidic Protein - metabolism | Ocular Hypertension - drug therapy | Gliosis - pathology | Mitogen-Activated Protein Kinase 1 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Ependymoglial Cells - pathology | Disease Models, Animal | Barium Compounds - administration & dosage | Butadienes - pharmacology | Gliosis - genetics | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Ocular Hypertension - pathology | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | Proto-Oncogene Proteins c-fos - metabolism | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Potassium Channels, Inwardly Rectifying - genetics | Ependymoglial Cells - drug effects | Rats, Sprague-Dawley | Ocular Hypertension - genetics | Cyclic AMP Response Element-Binding Protein - genetics | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Chlorides - administration & dosage | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cyclic AMP Response Element-Binding Protein - metabolism | Proto-Oncogene Proteins c-fos - genetics | Gliosis - drug therapy | Protein Kinase Inhibitors - pharmacology | Chronic Disease | Potassium Channels, Inwardly Rectifying - metabolism | Retina - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Transcription factors | Potassium channels (inwardly-rectifying) | P elements | Glial fibrillary acidic protein | c-Jun protein | Extracellular signal-regulated kinase | MAP kinase | Retina | Injection | Cyclic AMP response element-binding protein | Kinases | Proteins | Signal transduction | Gliosis | Protein kinase | Rodents | c-Fos protein | Glutamic acid receptors (metabotropic)
Journal Article
by Li, H and Xu, H and Zhou, Y and Zhang, J and Long, C and Li, S and Chen, S and Zhou, J.-M and Shao, F
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2007, Volume 315, Issue 5814, pp. 1000 - 1003
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 5, p. e97675
.... We previously showed that Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) activation with bacterial peptidoglycan... 
ACTIVATION | OBESITY | RECOGNITION | MECHANISM | INSULIN-RESISTANCE | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | ENDOTOXEMIA | MICROBIOTA | NF-KAPPA-B | EXPRESSION | Lipolysis - drug effects | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gonads - drug effects | Nod1 Signaling Adaptor Protein - deficiency | Adipose Tissue - cytology | Adipocytes - cytology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | NF-kappa B - metabolism | Adipocytes - drug effects | Adipose Tissue - metabolism | Gonads - cytology | Cyclic AMP-Dependent Protein Kinases - genetics | Mitogen-Activated Protein Kinase 1 - genetics | JNK Mitogen-Activated Protein Kinases - genetics | Cyclic AMP-Dependent Protein Kinases - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | 3T3-L1 Cells | Mice, Knockout | Gonads - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | NF-kappa B - genetics | Adipocytes - metabolism | Mitogen-Activated Protein Kinases - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Peptidoglycan - pharmacology | Adipose Tissue - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Nod1 Signaling Adaptor Protein - genetics | Obesity | Metabolites | Insulin resistance | Inflammation | Lipase | Phosphotransferases | Protein binding | Protein kinase A | Pediatrics | Transcription factors | Adipose tissue | Pollution load | Lipids | Activation | Biochemistry | Hormones | Adipocytes | Glucose | Kinases | Defects | Proteins | Receptors | Microbiota | Nutrient loading | Rodents | Animal tissues | Bacteria | Inhibition | Nod1 protein | Endotoxemia | Explants | Cues | Pathogens | NF-κB protein | Oligomerization | Cytokines | Hyperlipidemia | Peptidoglycans | Extracellular signal-regulated kinase | c-Jun protein | Glycerol | MAP kinase | Metabolism | Insulin | Lipolysis | Ligands
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2009, Volume 284, Issue 19, pp. 13165 - 13173
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 microglia to inflammatory sites in several neurological diseases... 
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
Blood, ISSN 0006-4971, 07/2004, Volume 104, Issue 1, pp. 256 - 262
.... On the other hand, the p42/p44 mitogen-activated protein kinase (MAPK) pathway activates uPA gene expression through Sp1 phosphorylation in HeLa, LNCaP, and CCL39-derivative cells... 
UROKINASE EXPRESSION | AP-1 SITES | PLASMINOGEN-ACTIVATOR | SIGNALING PATHWAY | ENHANCER | INDUCTION | C-JUN | HEMATOLOGY | BINDING | PROTEIN-KINASES | ENDOTHELIAL GROWTH-FACTOR | Phosphorylation | Cricetulus | Nitriles - pharmacology | Humans | Transcriptional Activation - drug effects | Sp1 Transcription Factor - metabolism | Promoter Regions, Genetic - genetics | MAP Kinase Signaling System | Dose-Response Relationship, Drug | RNA, Messenger - biosynthesis | Mitogen-Activated Protein Kinase 1 - genetics | JNK Mitogen-Activated Protein Kinases | Fibroblasts - metabolism | Recombinant Proteins - metabolism | Butadienes - pharmacology | Cricetinae | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Genes, Reporter - genetics | Recombinant Proteins - genetics | Urokinase-Type Plasminogen Activator - genetics | Animals | Mitogen-Activated Protein Kinase 1 - pharmacology | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - pharmacology | Cell Line, Tumor | Mitogen-Activated Protein Kinases - genetics | Urokinase-Type Plasminogen Activator - biosynthesis | Fibroblasts - cytology | HeLa Cells | Enzyme Activation - genetics | Mitogen-Activated Protein Kinase 3 | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Enzyme Inhibitors | Recombinant Proteins | Urinary Plasminogen Activator | Life Sciences | Fibroblasts | Nitriles | Sp1 Transcription Factor | Genes, Reporter | Mitogen-Activated Protein Kinases | Promoter Regions (Genetics) | Trans-Activation (Genetics) | Biochemistry, Molecular Biology | Butadienes | Enzyme Activation | Mitogen-Activated Protein Kinase 1 | Molecular biology | RNA, Messenger | Hela Cells | Cancer
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 2016, Volume 36, Issue 6, pp. 1122 - 1131
OBJECTIVE—The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling... 
atherosclerosis | apoptosis | macrophages | MAP kinase signaling system | endoplasmic reticulum stress | SURVIVAL | ACTIVATION | PHOSPHORYLATION | BAD | SIGNAL-TRANSDUCTION | OBESITY | NH2-TERMINAL KINASE (JNK)1 | INSULIN-RESISTANCE | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | REQUIREMENT | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Apoptosis - drug effects | Bone Marrow Cells - enzymology | Atherosclerosis - genetics | Mitogen-Activated Protein Kinase 9 - genetics | PTEN Phosphohydrolase - antagonists & inhibitors | Atherosclerosis - enzymology | Hypercholesterolemia - enzymology | Diet, High-Fat | Bone Marrow Transplantation | Receptors, LDL - deficiency | bcl-Associated Death Protein - metabolism | Bone Marrow Cells - drug effects | Mitogen-Activated Protein Kinase 8 - genetics | Aortic Diseases - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Macrophages - pathology | Signal Transduction | Cell Survival | Aorta - drug effects | Mice, Inbred C57BL | Bone Marrow Cells - pathology | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Plaque, Atherosclerotic | Mitogen-Activated Protein Kinase 9 - deficiency | Macrophages - enzymology | Mice, Knockout | Aorta - pathology | Mitogen-Activated Protein Kinase 8 - deficiency | Aortic Diseases - genetics | Phenotype | Animals | Endoplasmic Reticulum Stress | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Macrophages - drug effects | Protein Kinase Inhibitors - pharmacology | Hypercholesterolemia - genetics
Journal Article
Nature (London), ISSN 1476-4687, 2017, Volume 550, Issue 7674, pp. 133 - 136
.... p21-activated kinases (PAKs) become activated in cells with acquired drug resistance and have a... 
METASTATIC MELANOMA | MEK | EPITHELIAL-CELLS | PHOSPHORYLATION | PATHWAY | RAF | P21-ACTIVATED-KINASE-1 | MULTIDISCIPLINARY SCIENCES | KINASE | MECHANISMS | THERAPIES | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | p21-Activated Kinases - antagonists & inhibitors | Melanoma - enzymology | JNK Mitogen-Activated Protein Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Proto-Oncogene Proteins c-raf - chemistry | Female | beta Catenin - chemistry | Phosphorylation - drug effects | p21-Activated Kinases - genetics | JNK Mitogen-Activated Protein Kinases - chemistry | Enzyme Activation - drug effects | p21-Activated Kinases - metabolism | beta Catenin - metabolism | Proto-Oncogene Proteins c-raf - metabolism | Mitogen-Activated Protein Kinase Kinases - chemistry | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Drug Resistance, Neoplasm - drug effects | Melanoma | Physiological aspects | Cellular signal transduction | Drug resistance | Observations | Health aspects | Mitogen-activated protein kinases | TOR protein | Therapy | Phosphorylation | Activation | Metastasis | Drug development | Kinases | Cancer therapies | Metastases | Proteins | β-catenin | Signal transduction | Inhibition | Extracellular signal-regulated kinase | MAP kinase | JNK protein | Patients | Signaling | Protein arrays | Molecular modelling | Biopsy | Cell lines | Apoptosis
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 2008, Volume 135, Issue 4, pp. 1311 - 1321
.... Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase family and is important for stress-induced JNK activation... 
Gastroenterology and Hepatology | JNK ACTIVATION | APOPTOSIS | GAMMA-RADIATION | PROTEIN-KINASE | MAP KINASES | TNF-ALPHA | STRESS | GASTROENTEROLOGY & HEPATOLOGY | ISOLATED MOUSE HEPATOCYTES | CELL-DEATH | INDUCED HEPATOTOXICITY | Drug Overdose - metabolism | Hepatocytes - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Mitogen-Activated Protein Kinase 9 - genetics | Drug Overdose - pathology | Acetaminophen - poisoning | Mitogen-Activated Protein Kinase 8 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinase 5 - metabolism | Chemical and Drug Induced Liver Injury - pathology | Disease Models, Animal | Drug Overdose - physiopathology | MAP Kinase Kinase Kinase 5 - genetics | Mitogen-Activated Protein Kinase 9 - metabolism | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 8 - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Chemical and Drug Induced Liver Injury - physiopathology | Mice, Knockout | Gene Expression Regulation, Enzymologic | Animals | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Signal Transduction - physiology | Mice | Analgesics, Non-Narcotic - poisoning | Hepatocytes - enzymology | Liver diseases | Protein kinases | Liver | Glutathione | Apoptosis | Index Medicus | Abridged Index Medicus
Journal Article
BMC genomics, ISSN 1471-2164, 11/2011, Volume 12, Issue 1, pp. 574 - 574
Journal Article