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1. Full Text The molecular, temporal and region-specific requirements of the beta isoform of Calcium/Calmodulin-dependent protein kinase type 2 (CAMK2B) in mouse locomotion
by Kool, Martijn J and Van De Bree, Jolet E and Bodde, Hanna E and Elgersma, Ype and Van Woerden, Geeske M
Scientific Reports, ISSN 2045-2322, 05/2016, Volume 6, Issue 1, p. 26989
Genetic approaches using temporal and brain region-specific restricted gene deletions have provided a wealth of insight in the brain regions and temporal... 
CEREBELLAR PURKINJE | FOREBRAIN | GENE | SYNAPSES | CRE RECOMBINASE EXPRESSION | BEHAVIOR | MULTIDISCIPLINARY SCIENCES | MICE | MOTOR COORDINATION | SYNAPTIC PLASTICITY | ALPHA-CAMKII | Calmodulin - genetics | Calcium - metabolism | Male | Corpus Striatum - metabolism | Spatial Learning - physiology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - deficiency | Female | Prosencephalon - metabolism | Prosencephalon - physiopathology | Gene Expression | Calmodulin - metabolism | Corpus Striatum - physiopathology | Isoenzymes - genetics | Cerebellum - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Cerebellum - physiopathology | Isoenzymes - deficiency | Association Learning - physiology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Rotarod Performance Test | Animals | Brain Mapping | Mice | Mutation
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2. Full Text Ca2+/Calmodulin-Dependent Protein Kinase II and Protein Kinase A Differentially Regulate Sarcoplasmic Reticulum Ca2+ Leak in Human Cardiac Pathology
by Fischer, Thomas H and Herting, Jonas and Tirilomis, Theodor and Renner, André and Neef, Stefan and Toischer, Karl and Ellenberger, David and Förster, Anna and Schmitto, Jan D and Gummert, Jan and Schöndube, Friedrich A and Hasenfuss, Gerd and Maier, Lars S and Sossalla, Samuel
Circulation, ISSN 0009-7322, 08/2013, Volume 128, Issue 9, pp. 970 - 981
BACKGROUND—Sarcoplasmic reticulum (SR) Ca leak through ryanodine receptor type 2 (RyR2) dysfunction is of major pathophysiological relevance in human heart... 
Heart failure | Calcium calmodulin-dependent protein kinase type 2 | Sarcoplasmic reticulum | Protein kinases | Hypertrophy | heart failure | RYANODINE RECEPTOR PHOSPHORYLATION | CARDIAC & CARDIOVASCULAR SYSTEMS | CONTRACTILITY | hypertrophy | protein kinases | VENTRICULAR MYOCYTES | RELEASE | FAILING HEARTS | calcium-calmodulin-dependent protein kinase type 2 | sarcoplasmic reticulum | ATRIAL-FIBRILLATION | CAMKII | CALCIUM SPARKS | PKA PHOSPHORYLATION | PERIPHERAL VASCULAR DISEASE | HEART-FAILURE PROGRESSION | Phosphorylation | Calcium - metabolism | Humans | Middle Aged | Homeostasis | Cardiomegaly - pathology | Male | Ryanodine Receptor Calcium Release Channel - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - drug effects | Case-Control Studies | Myocardium - metabolism | Female | Sarcoplasmic Reticulum - metabolism | Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors | Cyclic AMP-Dependent Protein Kinases - drug effects | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Cyclic AMP-Dependent Protein Kinases - metabolism | Enzyme Inhibitors - pharmacology | Myocardium - pathology | Heart Failure - metabolism | Heart Failure - pathology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | Disease Progression | Aged | Cardiomegaly - metabolism | Physiological aspects | Calcium channels | Research
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3. Full Text The lysosome rupture-activated TAK1-JNK pathway regulates NLRP3 inflammasome activation
by Okada, Masahiro and Matsuzawa, Atsushi and Yoshimura, Akihiko and Ichijo, Hidenori
Journal of Biological Chemistry, ISSN 0021-9258, 11/2014, Volume 289, Issue 47, pp. 32926 - 32936
Lysosome rupture triggers NLRP3 inflammasome activation in macrophages. However, the underlying mechanism is not fully understood. Here we showed that the... 
APOPTOSIS | TRANSLOCATION | OXIDATIVE STRESS | IL-1 SIGNALING PATHWAY | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIA | CRYSTALS | KINASE CASCADE | I-KAPPA-B | CELL-DEATH | Inflammasomes - metabolism | Calcium - metabolism | Cytoskeletal Proteins - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Protein Multimerization | Immunoblotting | JNK Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Signaling System | DNA-Binding Proteins - metabolism | Lysosomes - metabolism | RNA Interference | HEK293 Cells | Cytoskeletal Proteins - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | MAP Kinase Kinase Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Cytoskeletal Proteins - chemistry | DNA-Binding Proteins - genetics | Carrier Proteins - genetics | Carrier Proteins - metabolism | CARD Signaling Adaptor Proteins | Cell Line, Tumor | Enzyme Activation | Microscopy, Fluorescence | Lysosome Rupture | Signal Transduction | TAK1 | siRNA Screen | c-Jun N-terminal Kinase (JNK) | Ca2 | Mitogen-activated Protein Kinase (MAPK) | Innate Immunity | NLRP3 | Inflammasome | Calmodulin-dependent Protein Kinase II (CaMKII)
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4. Full Text Calmodulin-Dependent Protein Kinase II: Linking Heart Failure and Arrhythmias
by Swaminathan, Paari Dominic and Purohit, Anil and Hund, Thomas J and Anderson, Mark E
Circulation Research, ISSN 0009-7330, 06/2012, Volume 110, Issue 12, pp. 1661 - 1677
Understanding relationships between heart failure and arrhythmias, important causes of suffering and sudden death, remains an unmet goal for biomedical... 
Heart failure | Calmodulin-dependent protein kinase II | Ion channels | Remodeling | Arrhythmias | heart failure | METHIONINE SULFOXIDE REDUCTASE | remodeling | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | SUDDEN-DEATH | CARDIAC RYANODINE RECEPTOR | DILATED CARDIOMYOPATHY | calmodulin-dependent protein kinase II | ion channels | SIGNAL-TRANSDUCTION | arrhythmias | SARCOPLASMIC-RETICULUM CA2 | LEFT-VENTRICULAR DYSFUNCTION | PERIPHERAL VASCULAR DISEASE | MULTIFUNCTIONAL CAM KINASE | HEMATOLOGY | HUMAN ATRIAL MYOCYTES | Arrhythmias, Cardiac - pathology | Animals | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - physiology | Heart Failure - enzymology | Humans | Myocardial Contraction - physiology | Heart Failure - physiopathology | Arrhythmias, Cardiac - enzymology | Heart Failure - pathology | Arrhythmias, Cardiac - physiopathology
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5. Full Text Kinase-Catalyzed Modification of Gold Nanoparticles:  A New Approach to Colorimetric Kinase Activity Screening
by Wang, Zhenxin and Lévy, Raphaël and Fernig, David G and Brust, Mathias
Journal of the American Chemical Society, ISSN 0002-7863, 02/2006, Volume 128, Issue 7, pp. 2214 - 2215
Peptide-stabilized gold nanoparticles have been enzymatically biotinylated by a kinase-catalyzed reaction using biotin-ATP as a cosubstrate. Upon mixing with... 
ORGANIZATION | STREPTAVIDIN | PARTICLES | MECHANISM | DNA | SYSTEMS | HYBRIDIZATION | INHIBITORS | CHEMISTRY, MULTIDISCIPLINARY | AGGREGATION | ENZYMATIC MANIPULATION | Cyclic AMP-Dependent Protein Kinases - metabolism | Gold - chemistry | Colorimetry - methods | Phosphorylation | Biotinylation | Peptides - chemistry | Cyclic AMP-Dependent Protein Kinases - chemistry | Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors | Spectrophotometry, Ultraviolet | Avidin - metabolism | Calcium-Calmodulin-Dependent Protein Kinases - chemistry | Peptides - metabolism | Protein Kinase Inhibitors - analysis | Nanostructures - chemistry | Avidin - chemistry | Protein Kinase Inhibitors - pharmacology | Catalysis | Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors | Calcium-Calmodulin-Dependent Protein Kinase Type 2 | Calcium-Calmodulin-Dependent Protein Kinases - metabolism | Gold compounds | Biotin | Chemical properties | Structure | Protein kinases
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6. Full Text A Mechanism for Tunable Autoinhibition in the Structure of a Human Ca2+/Calmodulin-Dependent Kinase II Holoenzyme
by Chao, LH and Stratton, MM and Lee, IH and Rosenberg, OS and Levitz, J and Mandell, DJ and Kortemme, T and Groves, JT and Schulman, H and Kuriyan, J
CELL, ISSN 0092-8674, 09/2011, Volume 146, Issue 5, pp. 732 - 745
Calcium/calmodulin-dependent kinase II (CaMKII) forms a highly conserved dodecameric assembly that is sensitive to the frequency of calcium pulse trains.... 
INHIBITORY AUTOPHOSPHORYLATION | IN-VITRO | ACTIVATION | CALMODULIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEPENDENT PROTEIN-KINASE | RAY SOLUTION SCATTERING | ALPHA | CAM KINASE | CA2+ OSCILLATIONS | BRAIN | CELL BIOLOGY | Protein Structure, Tertiary | Amino Acid Sequence | Sequence Alignment | Animals | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - chemistry | Holoenzymes - metabolism | Humans | Models, Molecular | Crystallography, X-Ray | Holoenzymes - chemistry | Protein Conformation | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
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7. Full Text Activation of Calcium/Calmodulin-Dependent Protein Kinase II in Obesity Mediates Suppression of Hepatic Insulin Signaling
by Ozcan, Lale and Cristina de Souza, Jane and Harari, Alp Avi and Backs, Johannes and Olson, Eric N and Tabas, Ira
Cell Metabolism, ISSN 1550-4131, 12/2013, Volume 18, Issue 6, pp. 803 - 815
A hallmark of obesity is selective suppression of hepatic insulin signaling (“insulin resistance”), but critical gaps remain in our understanding of the... 
SKELETAL-MUSCLE | LIPID-METABOLISM | TRIBBLES HOMOLOG | PHOSPHORYLATION | LIVER | ENDOCRINOLOGY & METABOLISM | RESISTANCE | TRB3 EXPRESSION | MICE | ENDOPLASMIC-RETICULUM STRESS | GLUCOSE-PRODUCTION | CELL BIOLOGY | Mitogen-Activated Protein Kinase 14 - antagonists & inhibitors | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Hepatocytes - metabolism | Hepatocytes - cytology | Mitogen-Activated Protein Kinase 14 - metabolism | Palmitates - pharmacology | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Hepatocytes - drug effects | Protein-Serine-Threonine Kinases - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Insulin - pharmacology | Endoplasmic Reticulum Stress - drug effects | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Mice, Transgenic | Mitogen-Activated Protein Kinase 14 - genetics | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | Mice, Knockout | Obesity - metabolism | Obesity - pathology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Insulin - metabolism | Animals | Mice, Obese | Mice | Type 2 diabetes | Obesity | Insulin resistance | Protein kinases | Insulin | Cells
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8. Full Text The δ Isoform of Cam Kinase II Is Required for Pathological Cardiac Hypertrophy and Remodeling after Pressure Overload
by Johannes Backs and Thea Backs and Stefan Neef and Michael M. Kreusser and Lorenz H. Lehmann and David M. Patrick and Chad E. Grueter and Xiaoxia Qi and James A. Richardson and Joseph A. Hill and Hugo A. Katus and Rhonda Bassel-Duby and Lars S. Maier and Eric N. Olson
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2009, Volume 106, Issue 7, pp. 2342 - 2347
Acute and chronic injuries to the heart result in perturbation of intracellular calcium signaling, which leads to pathological cardiac hypertrophy and... 
Protein isoforms | Heart | Pathology | Cardiomegaly | Phosphorylation | Exons | Polycystic kidney diseases | Histones | Renovations | Hypertrophy | Calcium signaling | CaM kinase II inhibitory peptide (AC3-I) | Excitation contraction coupling (EC coupling) | Thoracic aortic constriction (TAC) | Histone deacetylase 4 (HDAC4) | ACTIVATION | MULTIDISCIPLINARY SCIENCES | calcium signaling | SIGNALS | histone deacetylase 4 (HDAC4) | excitation contraction coupling (EC coupling) | DILATED CARDIOMYOPATHY | CaM Kinase II inhibitory peptide (AC3-I) | CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE | thoracic aortic constriction (TAC) | INACTIVATION | HEART-DISEASE | TRANSCRIPTION FACTOR | EXPRESSION | HISTONE DEACETYLASE-5 | CA2+ OSCILLATIONS | Signal Transduction | Calcium - metabolism | Cardiomegaly - pathology | Histone Deacetylases - metabolism | Protein Kinase C - antagonists & inhibitors | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | Mice, Knockout | Myocardial Infarction | Animals | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - chemistry | Models, Biological | Protein Kinase C - metabolism | Recombination, Genetic | Protein Isoforms | Mice | Models, Genetic | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Biological Sciences
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9. Full Text Crucial Role for Ca2+/Calmodulin-Dependent Protein Kinase-II in Regulating Diastolic Stress of Normal and Failing Hearts via Titin Phosphorylation
by Hamdani, N and Krysiak, J and Kreusser, M.M and Neef, S and dos Remedios, C.G and Maier, L.S and Kruger, M and Backs, J and Linke, W.A
Circulation Research, ISSN 0009-7330, 2013, Volume 112, Issue 4, pp. 664 - 674
RATIONALE:Myocardial diastolic stiffness and cardiomyocyte passive force (Fpassive) depend in part on titin isoform composition and phosphorylation.... 
calmodulin-dependent protein kinase-II | phosphoproteomics | titin | passive stiffness | diastolic function | Ca2+/calmodulin-dependent protein kinase-II | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | MUSCLE | ISOFORM | DILATED CARDIOMYOPATHY | FAILURE | CAMKII | CARDIAC-HYPERTROPHY | IN-VIVO | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | HEMATOLOGY | Protein Kinases - metabolism | Phosphorylation | Connectin | Compliance | Heart Failure - enzymology | Humans | Heart Failure - physiopathology | Recombinant Fusion Proteins - physiology | Molecular Sequence Data | Myocytes, Cardiac - enzymology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - deficiency | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - physiology | Muscle Proteins - metabolism | Protein Structure, Tertiary | Amino Acid Sequence | Cells, Cultured - drug effects | Rats | Mice, Transgenic | Diastole - physiology | Phosphoserine - metabolism | Phosphothreonine - metabolism | Mice, Knockout | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Biomechanical Phenomena | Animals | Myocytes, Cardiac - physiology | Cells, Cultured - metabolism | Mice | Protein Processing, Post-Translational
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10. Full Text Improving FRET dynamic range with bright green and red fluorescent proteins
by Lam, Amy J and St-Pierre, François and Gong, Yiyang and Marshall, Jesse D and Cranfill, Paula J and Baird, Michelle A and McKeown, Michael R and Wiedenmann, Jörg and Davidson, Michael W and Schnitzer, Mark J and Tsien, Roger Y and Lin, Michael Z
Nature Methods, ISSN 1548-7091, 10/2012, Volume 9, Issue 10, pp. 1005 - 1012
A variety of genetically encoded reporters use changes in fluorescence (or Forster) resonance energy transfer (FRET) to report on biochemical processes in... 
VISUALIZATION | ACTIVATION | CI-VSP | EXCITATION | KINASE | BIOCHEMICAL RESEARCH METHODS | RHO | SENSOR | CELL | LIFETIME | PROBES | Cyclic AMP-Dependent Protein Kinases - metabolism | Base Sequence | Humans | HEK293 Cells | Luminescent Proteins - chemistry | Molecular Sequence Data | Fluorescence Resonance Energy Transfer - methods | rhoA GTP-Binding Protein - metabolism | HeLa Cells | Green Fluorescent Proteins - chemistry | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Luminescent Proteins - metabolism | Genetic aspects | Properties | Neurons | Fluorescent proteins | Fluorescence microscopy | Methods | Proteins | Fluorescence | Biochemistry | Cellular biology
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11. Full Text Phosphorylation of synaptic GTPase-activating protein (synGAP) by Ca2 + /Calmodulin-dependent protein kinase II (CaMKII) and cyclin-dependent kinase 5 (CDK5) alters the ratio of its GAP activity toward ras and rap GTPases
by Walkup, Ward G and Washburn, Lorraine and Sweredoski, Michael J and Carlisle, Holly J and Graham, Robert L and Hess, Sonja and Kennedy, Mary B
Journal of Biological Chemistry, ISSN 0021-9258, 02/2015, Volume 290, Issue 8, pp. 4908 - 4927
synGAP is a neuron-specific Ras and Rap GTPase-activating protein (GAP) found in high concentrations in the postsynaptic density (PSD) fraction from the... 
NMDA RECEPTOR | DOMAIN | STIMULATION | INHIBITION | CALPAIN | CLONING | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTATIONS | HIPPOCAMPAL-NEURONS | PLASTICITY | Oncogene Proteins - genetics | ras Proteins - genetics | Phosphorylation | ras GTPase-Activating Proteins - chemistry | rap1 GTP-Binding Proteins - chemistry | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Receptors, N-Methyl-D-Aspartate - metabolism | ras Proteins - metabolism | Neurons - cytology | GTPase-Activating Proteins - metabolism | Receptors, N-Methyl-D-Aspartate - genetics | Cyclin-Dependent Kinase 5 - chemistry | Cyclin-Dependent Kinase 5 - genetics | ras GTPase-Activating Proteins - genetics | Receptors, N-Methyl-D-Aspartate - chemistry | ras Proteins - chemistry | Proto-Oncogene Proteins p21(ras) - chemistry | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | rap1 GTP-Binding Proteins - metabolism | ras GTPase-Activating Proteins - metabolism | Oncogene Proteins - chemistry | Cells, Cultured | Oncogene Proteins - metabolism | Rats | Synapses - enzymology | GTPase-Activating Proteins - chemistry | Cyclin-Dependent Kinase 5 - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Animals | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - chemistry | Neurons - enzymology | GTPase-Activating Proteins - genetics | rap1 GTP-Binding Proteins - genetics | rap GTP-Binding Proteins | Ras Protein | Ras-related Protein 1 (Rap1) | Postsynaptic Density | Ca2 | Synaptic Plasticity | Small GTPase | Neurobiology | Mass Spectrometry (MS) | Cyclin-dependent Kinase 5 (CDK5) | Protein Kinase | Calmodulin-dependent Protein Kinase II (CaMKII) | Synaptic GTPase-activating Protein (synGAP)
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12. Full Text Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model
by Wang, Junqin and Liu, Jiluo and Pan, Leilei and Qi, Ruirui and Liu, Peng and Zhou, Wei and Cai, Yiling
Scientific Reports, ISSN 2045-2322, 02/2017, Volume 7, Issue 1, p. 43385
Sensory mismatch between actual motion information and anticipated sensory patterns (internal model) is the etiology of motion sickness (MS). Some evidence... 
BILATERAL VESTIBULAR DEAFFERENTATION | DORSAL HIPPOCAMPUS | PLACE CELLS | MULTIDISCIPLINARY SCIENCES | ELEMENT-BINDING PROTEIN | SPATIAL MEMORY | THETA-RHYTHM | KNOCKOUT MICE | SYNAPTIC PLASTICITY | PROTEIN-KINASE-II | ALPHA-CAMKII | Otolithic Membrane - metabolism | Nitriles - pharmacology | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - metabolism | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Male | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - genetics | CREB-Binding Protein - genetics | Otolithic Membrane - pathology | CA1 Region, Hippocampal - pathology | CREB-Binding Protein - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Motion Sickness - physiopathology | CA1 Region, Hippocampal - metabolism | Otolithic Membrane - physiopathology | Phosphorylation - drug effects | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Disease Models, Animal | Motion Sickness - genetics | Butadienes - pharmacology | Mitogen-Activated Protein Kinase 3 - genetics | Motion Sickness - metabolism | Signal Transduction | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Motion Sickness - pathology | Gene Expression Regulation | Rats | Sulfonamides - pharmacology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | Rats, Sprague-Dawley | Rotation | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Mice | CA1 Region, Hippocampal - physiopathology | Benzylamines - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | Phosphorylation | Ca2+/calmodulin-dependent protein kinase IV | Otoliths | Extracellular signal-regulated kinase | Retention | Cyclic AMP response element-binding protein | Habituation | Signal transduction | Etiology | Motion sickness | Ca2+/calmodulin-dependent protein kinase | Vestibular system | Hippocampus | Ca2+/calmodulin-dependent protein kinase II
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13. Full Text Structure of the Autoinhibited Kinase Domain of CaMKII and SAXS Analysis of the Holoenzyme
by Rosenberg, Oren S and Deindl, Sebastian and Sung, Rou-Jia and Nairn, Angus C and Kuriyan, John and Argonne National Lab. (ANL), Argonne, IL (United States). Advanced Photon Source (APS)
Cell, ISSN 0092-8674, 12/2005, Volume 123, Issue 5, pp. 849 - 860
Ca /calmodulin-dependent protein kinase-II (CaMKII) is unique among protein kinases for its dodecameric assembly and its complex response to Ca . The crystal... 
SITE | BIOLOGICAL MACROMOLECULES | CRYSTAL-STRUCTURE | CALMODULIN | SUBSTRATE | BIOCHEMISTRY & MOLECULAR BIOLOGY | SOLUTION SCATTERING | DEPENDENT PROTEIN-KINASE | ALPHA | AUTOPHOSPHORYLATION | SUBUNIT | CELL BIOLOGY | Protein Structure, Tertiary | Amino Acid Sequence | Calmodulin - metabolism | Calcium-Calmodulin-Dependent Protein Kinases - genetics | Protein Structure, Secondary | Calcium - metabolism | Caenorhabditis elegans Proteins - chemistry | Caenorhabditis elegans Proteins - metabolism | Models, Molecular | Molecular Sequence Data | Crystallography, X-Ray | Holoenzymes - chemistry | Calcium-Calmodulin-Dependent Protein Kinases - chemistry | Sequence Alignment | Animals | Holoenzymes - metabolism | Protein Structure, Quaternary | Holoenzymes - genetics | Binding Sites | Caenorhabditis elegans Proteins - genetics | Calcium-Calmodulin-Dependent Protein Kinase Type 2 | Dimerization | Caenorhabditis elegans - enzymology | Calcium-Calmodulin-Dependent Protein Kinases - metabolism | Enzymes | Threonine | Peptides | Analysis | Crystals | Structure | Protein kinases | Calmodulin | PEPTIDES | RESOLUTION | CRYSTAL STRUCTURE | PHOSPHOTRANSFERASES | MATERIALS SCIENCE | PROTEINS | RESIDUES | SCATTERING | THREONINE
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14. Full Text Oxidized CaMKII causes cardiac sinus node dysfunction in mice
by Swaminathan, Paari Dominic and Purohit, Anil and Soni, Siddarth and Voigt, Niels and Singh, Madhu V and Glukhov, Alexey V and Gao, Zhan and He, B. Julie and Luczak, Elizabeth D and Joiner, Mei-Ling A and Kutschke, William and Yang, Jinying and Donahue, J. Kevin and Weiss, Robert M and Grumbach, Isabella M and Ogawa, Masahiro and Chen, Peng-Sheng and Efimov, Igor and Dobrev, Dobromir and Mohler, Peter J and Hund, Thomas J and Anderson, Mark E
Journal of Clinical Investigation, ISSN 0021-9738, 08/2011, Volume 121, Issue 8, pp. 3277 - 3288
Sinus node dysfunction (SND) is a major public health problem that is associated with sudden cardiac death and requires surgical implantation of artificial... 
MEDICINE, RESEARCH & EXPERIMENTAL | PRESSURE-OVERLOAD | MATHEMATICAL-MODEL | RYANODINE RECEPTOR | INHIBITION PROTECTS | DILATED CARDIOMYOPATHY | CONGESTIVE-HEART-FAILURE | CALMODULIN KINASE-II | SINOATRIAL NODE | PACEMAKER CHANNEL | ATRIAL-FIBRILLATION | Biomarkers - metabolism | Reactive Oxygen Species | Angiotensin II - metabolism | Humans | Mice, Transgenic | Sinoatrial Node - pathology | Animals | Sick Sinus Syndrome - metabolism | Dogs | Oxygen - chemistry | NADPH Oxidases - genetics | Mice | Sick Sinus Syndrome - genetics | Electrocardiography - methods | Apoptosis | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Physiological aspects | Research | Heart diseases | Protein kinases | Risk factors | Angiotensin
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