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Journal of Biological Chemistry, ISSN 0021-9258, 05/2012, Volume 287, Issue 19, pp. 15395 - 15408
Cellular O-linked N-acetylglucosamine (O-GlcNAc) levels are modulated by two enzymes: uridine diphosphate-N-acetyl-D-glucosamine: polypeptidyltransferase (OGT)... 
STRUCTURAL INSIGHTS | NUCLEAR | GLCNACYLATION | MECHANISM | TETRATRICOPEPTIDE REPEATS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CYTOSOLIC PROTEINS | GLYCOSYLATION | NUCLEOCYTOPLASMIC PROTEINS | BETA | Phosphorylation | Membrane Glycoproteins - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - metabolism | Humans | N-Acetylglucosaminyltransferases - genetics | Substrate Specificity | tau Proteins - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - genetics | Acetylglucosamine - metabolism | Nuclear Pore Complex Proteins - genetics | tau Proteins - genetics | Mass Spectrometry | Protein-Arginine N-Methyltransferases - genetics | beta-N-Acetylhexosaminidases - genetics | Recombinant Proteins - metabolism | Nuclear Pore Complex Proteins - metabolism | beta-N-Acetylhexosaminidases - metabolism | Serine - genetics | Glycosylation | Recombinant Proteins - genetics | Serine - metabolism | Blotting, Western | N-Acetylglucosaminyltransferases - metabolism | Membrane Glycoproteins - genetics | Protein-Arginine N-Methyltransferases - metabolism | Proteins - genetics | Proteins - metabolism | Adaptor Proteins, Signal Transducing - genetics | Protein Processing, Post-Translational | Kinetics | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Index Medicus | Glycoside Hydrolases | Carbohydrate Glycoconjugate | Glycosyltransferases | Glycobiology and Extracellular Matrices | Carbohydrate | Glycoconjugate | Carbohydrate Biosynthesis | O-GlcNAc
Journal Article
Brain, ISSN 0006-8950, 05/2011, Volume 134, Issue 5, pp. 1293 - 1314
Amyotrophic lateral sclerosis is a relentless and devastating adult-onset neurodegenerative disease with no known cure. In mice with amyotrophic lateral... 
IL-4 | FoxP3 | regulatory T lymphocytes | inflammation | microglia | MOTOR-NEURONS | WILD-TYPE MICROGLIA | SPINAL-CORD | ANTIINFLAMMATORY CYTOKINE | NEUROSCIENCES | CLINICAL NEUROLOGY | INHERITED ALS | IMMUNE-SYSTEM | MOUSE MODEL | ANIMAL-MODEL | ALTERNATIVE ACTIVATION | PARKINSONS-DISEASE | T-Lymphocytes, Regulatory - metabolism | Superoxide Dismutase - genetics | Toll-Like Receptor 2 - genetics | Age Factors | Amyotrophic Lateral Sclerosis - physiopathology | Humans | Middle Aged | Male | RNA, Messenger - metabolism | DNA-Binding Proteins - deficiency | T-Lymphocytes, Regulatory - pathology | T-Lymphocytes, Regulatory - immunology | Lectins - metabolism | Flow Cytometry | Forkhead Transcription Factors - metabolism | Spinal Cord - pathology | Adult | Female | beta-N-Acetylhexosaminidases - genetics | Receptors, Chemokine - genetics | Cytokines - genetics | Disease Models, Animal | Cytokines - metabolism | Gene Expression Regulation - genetics | beta-N-Acetylhexosaminidases - metabolism | Amyotrophic Lateral Sclerosis - genetics | Mice, Inbred C57BL | Receptors, Chemokine - metabolism | Cells, Cultured | Gene Expression Regulation - physiology | Mice, Transgenic | Toll-Like Receptor 2 - metabolism | Amyotrophic Lateral Sclerosis - blood | Coculture Techniques - methods | Mutation - genetics | Disease Progression | Microglia | Amyotrophic Lateral Sclerosis - pathology | Animals | Analysis of Variance | Interleukin-2 Receptor alpha Subunit - metabolism | Lectins - genetics | Aged | Mice | CX3C Chemokine Receptor 1 | CD4 Antigens - metabolism | Index Medicus | Abridged Index Medicus | Amyotrophic lateral sclerosis | Original
Journal Article
European Journal of Immunology, ISSN 0014-2980, 06/2011, Volume 41, Issue 6, pp. 1742 - 1753
Alternatively activated macrophages are critical in host defense against parasites and are protective in inflammatory bowel disease, but contribute to... 
IL-4 | Alternatively activated macrophages | SHIP | M2 MACROPHAGES | C/EBP-BETA | ARGINASE | NITRIC-OXIDE SYNTHASE | IMMUNOLOGY | PHOSPHOINOSITIDE 3-KINASE | CUTTING EDGE | SIGNAL-TRANSDUCTION | GENE-EXPRESSION | TUMOR-ASSOCIATED MACROPHAGES | NF-KAPPA-B | RNA, Small Interfering - genetics | Transcriptional Activation - genetics | Macrophage Activation - genetics | Granulocyte-Macrophage Colony-Stimulating Factor - metabolism | Arginase - metabolism | Inositol Polyphosphate 5-Phosphatases | Phosphatidylinositol 3-Kinases - metabolism | STAT6 Transcription Factor - genetics | src Homology Domains - genetics | Phosphatidylinositol 3-Kinases - immunology | Lectins - metabolism | Phosphoric Monoester Hydrolases - immunology | beta-N-Acetylhexosaminidases - genetics | Macrophages - immunology | Biomarkers - metabolism | Phosphoric Monoester Hydrolases - genetics | Macrophages - pathology | beta-N-Acetylhexosaminidases - metabolism | Interleukin-4 - metabolism | Transgenes - genetics | Cells, Cultured | Arginase - genetics | Signal Transduction - genetics | STAT6 Transcription Factor - metabolism | Mice, Knockout | Neoplasms - drug therapy | Interleukin-4 - immunology | Macrophages - metabolism | Animals | Granulocyte-Macrophage Colony-Stimulating Factor - immunology | Neoplasms - immunology | Lectins - genetics | Mice | Neoplasms - pathology | Phosphoric Monoester Hydrolases - metabolism | Kinases | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 09/2016, Volume 291, Issue 36, pp. 18897 - 18914
O-GlcNAcylation is a dynamic post-translational modification consisting of the addition of a single N-acetylglucosamine sugar to serine and threonine residues... 
X-CHROMOSOME | GLCNACYLATION | TUMOR SUPPRESSION | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROTEIN MODIFICATION | TRANSCRIPTION | RESISTANCE | GLYCOSYLATION | HEXOSAMINE BIOSYNTHESIS | TRANSFERASE | Humans | Ovarian Neoplasms - pathology | Homeostasis | N-Acetylglucosaminyltransferases - genetics | Tumor Suppressor Protein p53 - genetics | Acetylglucosamine - metabolism | Ovarian Neoplasms - genetics | RNA, Messenger - biosynthesis | Cell Nucleus - metabolism | Cell Nucleus - pathology | Female | Ovarian Neoplasms - metabolism | beta-N-Acetylhexosaminidases - genetics | Active Transport, Cell Nucleus - genetics | Pyrans - pharmacology | beta-N-Acetylhexosaminidases - metabolism | RNA, Messenger - genetics | Gene Silencing | Tumor Suppressor Protein p53 - metabolism | beta-N-Acetylhexosaminidases - antagonists & inhibitors | Acetylglucosamine - genetics | N-Acetylglucosaminyltransferases - metabolism | RNA, Neoplasm - biosynthesis | Cell Nucleus - genetics | Active Transport, Cell Nucleus - drug effects | Protein Stability - drug effects | Cell Line, Tumor | RNA, Neoplasm - genetics | Protein Processing, Post-Translational | Thiazoles - pharmacology | Mutation | Index Medicus | O-linked N-acetylglucosamine (O-GlcNAc) | ovarian cancer | cell growth | O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT) | O-GlcNAcase | Glycobiology and Extracellular Matrices | p53
Journal Article
Nature Immunology, ISSN 1529-2908, 05/2016, Volume 17, Issue 5, pp. 538 - 544
Acidic mammalian chitinase (AMCase) is known to be induced by allergens and helminths, yet its role in immunity is unclear. Using AMCase-deficient mice, we... 
Strongylida Infections - metabolism | Hypersensitivity - immunology | Interleukin-13 - immunology | Hormones, Ectopic - metabolism | Chitinases - metabolism | Chloride Channels - genetics | Nippostrongylus - immunology | Nematospiroides dubius - immunology | Chitinases - genetics | Gastrointestinal Tract - immunology | Lectins - metabolism | Interleukin-13 - genetics | Flow Cytometry | Hypersensitivity - metabolism | Strongylida Infections - parasitology | Strongylida Infections - immunology | Gene Expression - immunology | Hypersensitivity - genetics | Lung - metabolism | beta-N-Acetylhexosaminidases - genetics | Nematospiroides dubius - physiology | Lung - pathology | Lectins - immunology | beta-N-Acetylhexosaminidases - metabolism | Mice, Inbred C57BL | Immunity - immunology | Host-Parasite Interactions - immunology | beta-N-Acetylhexosaminidases - immunology | Chloride Channels - immunology | Interleukin-13 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Gastrointestinal Tract - metabolism | Mice, Knockout | Chloride Channels - metabolism | Animals | Nippostrongylus - physiology | Hormones, Ectopic - immunology | Hormones, Ectopic - genetics | Chitinases - immunology | Lectins - genetics | Immunity - genetics | Gastrointestinal Tract - parasitology | Lung - immunology | Microscopy, Fluorescence | Roundworm infections | Enzymes | Immune response | Gastrointestinal diseases | Development and progression | Hydrolases | Genetic aspects | Properties | Index Medicus
Journal Article
Human Gene Therapy, ISSN 1043-0342, 06/2017, Volume 28, Issue 6, pp. 51 - 522
GM2 gangliosidoses, including Tay–Sachs disease and Sandhoff disease, are lysosomal storage disorders caused by deficiencies in β-N-acetylhexosaminidase (Hex).... 
Research Articles | hexosaminidase | gene therapy | adeno-associated virus | Tay-Sachs disease | intracranial delivery | AAV | LONG-TERM | MOUSE-BRAIN | MEDICINE, RESEARCH & EXPERIMENTAL | SINGLE INJECTION | SANDHOFF-DISEASE | VECTOR | DELIVERY | FELINE MODEL | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENETICS & HEREDITY | NERVOUS-SYSTEM DISEASE | GENE-THERAPY | REDUCES LYSOSOMAL STORAGE | Dependovirus - genetics | Neurons - pathology | Thalamus - metabolism | White Matter - metabolism | Injections, Intraventricular | Macaca fascicularis | Genetic Vectors - adverse effects | Male | Thalamus - pathology | Gangliosidoses, GM2 - pathology | Necrosis - pathology | Protein Subunits - metabolism | Apathy | Gray Matter - metabolism | Female | Neurons - metabolism | beta-N-Acetylhexosaminidases - genetics | Transgenes | Gangliosidoses, GM2 - genetics | Dyskinesias - genetics | Disease Models, Animal | Protein Subunits - genetics | Gangliosidoses, GM2 - therapy | Gene Expression | Dependovirus - metabolism | Genetic Vectors - chemistry | beta-N-Acetylhexosaminidases - metabolism | Dyskinesias - pathology | Genetic Vectors - metabolism | Necrosis - metabolism | Dyskinesias - etiology | Dyskinesias - metabolism | White Matter - pathology | Protein Subunits - adverse effects | Animals | Necrosis - etiology | Gray Matter - pathology | Necrosis - genetics | beta-N-Acetylhexosaminidases - adverse effects | Gangliosidoses, GM2 - metabolism | Genetic Therapy - methods | Neuroimaging | Brain | Hex protein | Central nervous system | Lysosomal storage diseases | Ventricles (cerebral) | Monkeys | Substantia grisea | Necrosis | Proteins | Infusion | Neurotoxicity | Histopathology | Coding | Ataxia | Thalamus | Safety | Lesions | Leukocytes (eosinophilic) | Abnormalities | Injection | Magnetic resonance imaging | Sheep | Ventricle | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 04/2016, Volume 36, Issue 15, pp. 4182 - 4195
Stroke is a leading cause of disability and currently lacks effective therapy enabling long-term functional recovery. Ischemic brain injury causes local... 
Neuroinflammation | Stroke | Monocyte | Macrophage | Microglia | FOCAL CEREBRAL-ISCHEMIA | macrophage | RECEPTOR | MICROGLIAL CELLS | stroke | NEUROSCIENCES | IMMUNE-SYSTEM | neuroinflammation | INFLAMMATORY CELLS | STAIRCASE TEST | monocyte | CENTRAL-NERVOUS-SYSTEM | CHEMOATTRACTANT PROTEIN-1 | RAT-BRAIN | microglia | ALTERNATIVE ACTIVATION | Infarction, Middle Cerebral Artery - physiopathology | Inflammation - pathology | Recovery of Function - drug effects | Antigens, CD - biosynthesis | Male | Antibodies, Blocking - pharmacology | Antigens, CD - genetics | Lectins - biosynthesis | Stroke - physiopathology | Transforming Growth Factor beta - biosynthesis | Receptors, CCR2 - antagonists & inhibitors | Stroke - pathology | Neuronal Plasticity - physiology | Monocytes - pathology | Behavior, Animal - drug effects | Receptors, Cell Surface - biosynthesis | beta-N-Acetylhexosaminidases - genetics | Antigens, Differentiation, Myelomonocytic - biosynthesis | Macrophages - pathology | Mice, Inbred C57BL | Psychomotor Performance - drug effects | Functional Laterality | beta-N-Acetylhexosaminidases - biosynthesis | Antigens, Differentiation, Myelomonocytic - genetics | Animals | Transforming Growth Factor beta - genetics | Lectins - genetics | Mice | Chimera | Receptors, Cell Surface - genetics | Index Medicus | Neurologi | Clinical Medicine | Neurology | Medical and Health Sciences | Medicin och hälsovetenskap | Klinisk medicin
Journal Article
Current Gene Therapy, ISSN 1566-5232, 2018, Volume 18, Issue 2, pp. 68 - 89
Journal Article
BBA - Molecular Basis of Disease, ISSN 0925-4439, 05/2015, Volume 1852, Issue 5, pp. 893 - 904
, the etiological agent of Chagas' disease, induces a persistent inflammatory response. Macrophages are a first line cell phenotype involved in the clearance... 
Inflammatory mediators | Macrophage polarization | PPAR | Trypanosoma cruzi | CELLS | LIPID-METABOLISM | BIOCHEMISTRY & MOLECULAR BIOLOGY | TISSUE | RECEPTOR | HUMAN MONOCYTES | BIOPHYSICS | GENE | NF-KAPPA-B | EXPRESSION | ALTERNATIVE ACTIVATION | ARGINASE INDUCTION | Chagas Disease - parasitology | Arginase - metabolism | Male | PPAR gamma - metabolism | Chagas Disease - metabolism | Lectins - metabolism | RNA Interference | Inflammation Mediators - metabolism | Prostaglandin D2 - analogs & derivatives | beta-N-Acetylhexosaminidases - genetics | Cytokines - genetics | PPAR gamma - genetics | Phagocytosis - drug effects | Macrophages - classification | Cytokines - metabolism | beta-N-Acetylhexosaminidases - metabolism | Cells, Cultured | PPAR alpha - genetics | Arginase - genetics | Pyrimidines - pharmacology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Trypanosoma cruzi - physiology | Host-Pathogen Interactions | Macrophages - metabolism | Animals | Transforming Growth Factor beta - genetics | Nitric Oxide Synthase Type II - genetics | Lectins - genetics | Ligands | Macrophages - drug effects | Mice, Inbred BALB C | Prostaglandin D2 - pharmacology | PPAR alpha - metabolism | Macrophage Activation - drug effects | Chagas Disease - genetics | Transforming Growth Factor beta - metabolism | Microscopy, Fluorescence | Nitric Oxide Synthase Type II - metabolism
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2010, Volume 107, Issue 6, pp. 2413 - 2418
In a globalized economy, the control of fruit ripening is of strategic importance because excessive softening limits shelf life. Efforts have been made to... 
Ripening | Enzymes | Cell walls | Genes | Shelf life | Gene expression regulation | Plants | Transgenic plants | Fruits | Plant cells | β-D-N-acetylhexosaminidase | Fruit softening | RNAi | α-mannosidase | TOMATO FRUIT | MULTIDISCIPLINARY SCIENCES | fruit softening | HEXOSAMINIDASE | LYCOPERSICON-ESCULENTUM | GENETIC-REGULATION | alpha-mannosidase | beta-D-N-acetylhexosaminidase | CELL-WALL METABOLISM | ANTISENSE RNA | MANNOSIDASE | PLANTS | EXPRESSION | EFFICIENT | alpha-Mannosidase - metabolism | DNA, Complementary - genetics | Molecular Sequence Data | Immunoblotting | Lycopersicon esculentum - enzymology | Fruit - enzymology | RNA Interference | Time Factors | Mass Spectrometry | Plants, Genetically Modified | Cloning, Molecular | Gene Expression Regulation, Plant | Lycopersicon esculentum - genetics | Plant Proteins - metabolism | beta-N-Acetylhexosaminidases - genetics | Fruit - metabolism | Fruit - genetics | Amino Acid Sequence | Lycopersicon esculentum - metabolism | beta-N-Acetylhexosaminidases - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Sequence Analysis, DNA | Gene Expression Regulation, Enzymologic | Plant Proteins - genetics | DNA, Complementary - chemistry | alpha-Mannosidase - genetics | Crops | Food conservation | Protection and preservation | Research | Oligosaccharides | Enzyme kinetics | Properties | Methods | Food | Proteins | Genetics | Biochemistry | Tomatoes | Ribonucleic acid--RNA | Index Medicus | Biological Sciences
Journal Article
PLoS Pathogens, ISSN 1553-7366, 07/2017, Volume 13, Issue 7, pp. e1006518 - e1006518
The viral Tax oncoprotein plays a key role in both Human T-cell lymphotropic virus type 1 (HTLV-1)-replication and HTLV-1-associated pathologies, notably adult... 
CREB PHOSPHORYLATION | RESONANCE ENERGY-TRANSFER | MICROBIOLOGY | BINDING PROTEIN | ENHANCER COMPLEX | TRANSACTIVATOR TAX | INSULIN-RECEPTOR | VIROLOGY | BETA-N-ACETYLGLUCOSAMINE | VIRUS TYPE-I | GENE-EXPRESSION | PARASITOLOGY | LIVING CELLS | T-Lymphocytes - enzymology | beta-N-Acetylhexosaminidases - metabolism | Humans | N-Acetylglucosaminyltransferases - genetics | Gene Products, tax - genetics | HTLV-I Infections - virology | N-Acetylglucosaminyltransferases - metabolism | T-Lymphocytes - virology | Acetylglucosamine - metabolism | Host-Pathogen Interactions | Cyclic AMP Response Element-Binding Protein - genetics | Gene Products, tax - metabolism | HTLV-I Infections - metabolism | T-Lymphocytes - metabolism | Gene Expression Regulation, Viral | Cyclic AMP Response Element-Binding Protein - metabolism | Human T-lymphotropic virus 1 - metabolism | Transcription, Genetic | Human T-lymphotropic virus 1 - genetics | Protein Processing, Post-Translational | beta-N-Acetylhexosaminidases - genetics | HTLV-I Infections - enzymology | HTLV-I Infections - genetics | Post-translational modification | Physiological aspects | Genetic aspects | Research | Genetic transcription | T cells | HTLV-I (Virus) | Biotechnology | Phosphorylation | Tax protein | Transcription | N-Acetylglucosamine | Leukemia | Serine | Viruses | Lymphocytes T | Regulatory sequences | Recruitment | Proteins | Lymphocytes | Post-translation | Enzymes | Co authorship | Threonine | Cyclic AMP | Pharmacology | Cyclic AMP response element-binding protein | Gene expression | Insulin | Cell lines | Dimers | Taxation | Index Medicus
Journal Article