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1. Full Text Identification of arrestin-3-specific residues necessary for JNK3 kinase activation
by Seo, Jungwon and Tsakem, Elviche L and Breitman, Maya and Gurevich, Vsevolod V
Journal of Biological Chemistry, ISSN 0021-9258, 08/2011, Volume 286, Issue 32, pp. 27894 - 27901
Arrestins bind active phosphorylated G protein-coupled receptors, blocking G protein activation and channeling the signaling to G protein-independent pathways.... 
WILD-TYPE | CLATHRIN ADAPTER | CRYSTAL-STRUCTURE | NONVISUAL ARRESTINS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CONE ARRESTIN | NUCLEAR EXPORT SIGNAL | PROTEIN-COUPLED RECEPTORS | BETA-ARRESTIN | BINDING | VISUAL ARRESTIN | Phosphorylation - physiology | Protein Structure, Tertiary | MAP Kinase Kinase Kinase 5 - genetics | Protein Structure, Secondary | Cercopithecus aethiops | Arrestins - genetics | Arrestins - metabolism | Mitogen-Activated Protein Kinase 10 - genetics | Mitogen-Activated Protein Kinase 10 - metabolism | Animals | Cattle | MAP Kinase Kinase Kinase 5 - metabolism | COS Cells | Enzyme Activation - physiology | Index Medicus | Site-directed Mutagenesis | MAP Kinases (MAPKs) | Signal Transduction | Jun N-terminal kinase (JNK) | Arrestin | G Protein-coupled Receptors (GPCRs) | Protein-Protein Interactions
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2. Full Text Progressive reduction of its expression in rods reveals two pools of Arrestin-1 in the outer segment with different roles in photoresponse recovery
by Cleghorn, Whitney M and Tsakem, Elviche L and Song, Xiufeng and Vishnivetskiy, Sergey A and Seo, Jungwon and Chen, Jeannie and Gurevich, Eugenia V and Gurevich, Vsevolod V
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 7, p. e22797
Light-induced rhodopsin signaling is turned off with sub-second kinetics by rhodopsin phosphorylation followed by arrestin-1 binding. To test the availability... 
MONOMERIC RHODOPSIN | MULTIPLE PHOSPHORYLATION | MOUSE RODS | DIRECT BINDING | PAIRED-FLASH ELECTRORETINOGRAMS | SIGNALING PROTEINS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | VISUAL ARRESTIN | PHOTORECEPTOR CELLS | LIVING CELLS | Animals | Rod Cell Outer Segment - metabolism | Time Factors | Light | Mice | Light Signal Transduction - radiation effects | Arrestin - metabolism | Rod Cell Outer Segment - radiation effects | Rhodopsin | Neurophysiology | Phosphorylation | Neurosciences | Diffusion rate | Dark adaptation | Retina | Arrestin | Rods | Rod outer segment membranes | Inactivation | Recovery | Proteins | Transgenic animals | Light intensity | Antigens | Deactivation | Desensitization | Photons | Pharmacology | Pools | Electroretinograms | Quenching | Luminous intensity | Signaling | Cytoskeleton | Photoreceptors | Kinetics
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3. Full Text Cognitive effects of dopamine depletion in the context of diminished acetylcholine signaling capacity in mice
by Zurkovsky, Lilia and Bychkov, Evgeny and Tsakem, Elviche L and Siedlecki, Carley and Blakely, Randy D and Gurevich, Eugenia V
DMM Disease Models and Mechanisms, ISSN 1754-8403, 01/2013, Volume 6, Issue 1, pp. 171 - 183
A subset of patients with Parkinson's disease acquires a debilitating dementia characterized by severe cognitive impairments (i.e. Parkinson's disease... 
PARKINSON-DISEASE DEMENTIA | ALZHEIMERS-DISEASE | IN-VIVO | ATTENTIONAL SET | LESIONED RATS | CORTICAL LEWY BODIES | PATHOLOGY | SUBSTANTIA-NIGRA | EARLY-PHASE | PREFRONTAL CORTEX | WORKING-MEMORY | CELL BIOLOGY | Dementia - psychology | Parkinsonian Disorders - complications | Cholinergic Agents - pharmacology | Humans | Dementia - physiopathology | Male | Acetylcholine - deficiency | Dopamine - deficiency | Membrane Transport Proteins - deficiency | Dopamine - physiology | Membrane Transport Proteins - genetics | Cognition Disorders - etiology | Cognition Disorders - psychology | Disease Models, Animal | Parkinsonian Disorders - physiopathology | Cognition Disorders - physiopathology | Signal Transduction | Mice, Inbred C57BL | Parkinsonian Disorders - psychology | Mice, Knockout | Dementia - etiology | Animals | Hemicholinium 3 - pharmacology | Mice | Acetylcholine - physiology | Memory - physiology
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