INT69484
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Overexpression of MOR1K in mammalian cells revealed that this 6TM receptor is not expressed at the cell membrane, but instead is retained in the intracellular compartment (Fig.1C). | |||||||||||||||
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Taken together, these findings suggest that activation of constitutively expressed MOR inhibits microglial cell chemotaxis and support the notion of an anti-inflammatory role of MOR within the brain. | |||||||||||||||
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The results of our study indicate that, in MCF-7 cells, MOR gene expression is downregulated by opioid agonists and upregulated by opioid antagonists. | |||||||||||||||
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Naloxone alone produced a slight increase in MOR gene expression. | |||||||||||||||
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The aim of the study was to investigate the presence of opioid receptor types in human breast adenocarcinoma MCF-7 cells and to characterize the changes in MOR expression induced by opioid agonist and antagonist treatment. | |||||||||||||||
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Retinoid-induced mu opioid receptor expression by phytohemagglutinin-stimulated U937 cells. | |||||||||||||||
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Retinoid X receptor (RXR) agonist and retinoic acid receptor (RAR) antagonist further increased MOR expression by the PHA-stimulated cells. | |||||||||||||||
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It was shown previously that MOP expression is not increased in PC12 cells exposed to ethanol [22], [27], suggesting that elevated MOP surface density is due to differences in trafficking and/or sorting of the existing pool of MOP. | |||||||||||||||
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We find that chronic exposure of human saphenous vein, atria and internal thoracic artery endothelium to the human immunodeficiency virus surface glycoprotein gp120, results in an increase in endothelial mu opioid receptor expression (52%). gp120 acts, in this regard, as a proinflammatory cytokine (e.g. interleukin-1-alpha) by increasing endothelial mu opioid receptor expression. | |||||||||||||||
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The MOR gene is tightly regulated at the level of transcription, and potential polymorphisms in its 5' regulatory region can cause individual variation in MOR gene expression, nociception, and opiate responses. | |||||||||||||||
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Real-time PCR indicated that the expression of MOR, DOR and KOR in hypertrophic scars was enhanced in comparison with normal skin. | |||||||||||||||
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Be2C cells transfected with either MOR1 or MOR1K retained a significantly higher proportion of fluorescently-labeled naloxone in comparison with cells transfected with an empty vector control. | |||||||||||||||
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A moderate increase in morphine-evoked Ca2+ levels was also observed in Be2C cells transfected with MOR1 or empty vector, however this was likely due to the high endogenous expression of MOR1K in this cell line (Fig.1B). | |||||||||||||||
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For MOR1 expressing cells, maximum NO production (7.5 pM) occurred at ~50 sec after administration of 1 ? | |||||||||||||||
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Since activation of MOR1K results in the intracellular accumulation of Ca2+ and showed a tendency to increase cAMP levels, we examined whether MOR1K couples to G? | |||||||||||||||
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Furthermore, COS1 cells transfected with MOR1K showed a substantial increase in intracellular Ca2+ release following morphine treatment, which was not observed in MOR1 expressing cells (Fig. 2B). | |||||||||||||||
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These data suggest that human MOR1K expression is restricted to neuronal cells. | |||||||||||||||
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For MOR1 expressing cells, maximum NO production (7.5 pM) occurred at ~50 sec after administration of 1 ? | |||||||||||||||
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Be2C cells transfected with either MOR1 or MOR1K retained a significantly higher proportion of fluorescently-labeled naloxone in comparison with cells transfected with an empty vector control. | |||||||||||||||
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RESULTS: In this study, we demonstrate that after 12h cold exposure (4 degrees C from 24 degrees C), the estimated relative mu opiate receptor (MOR) gene expression in M. edulis pedal ganglia, measured by real-time PCR, did not differ significantly from the control group (1.23+/-0.25, p>0.05). | |||||||||||||||
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