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PMID:10338466
| Citation |
Cho, MC, Rao, M, Koch, WJ, Thomas, SA, Palmiter, RD and Rockman, HA (1999) Enhanced contractility and decreased beta-adrenergic receptor kinase-1 in mice lacking endogenous norepinephrine and epinephrine. Circulation 99:2702-7 |
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| Abstract |
Elevated circulating norepinephrine (NE) has been implicated in causing the profound beta-adrenergic receptor (betaAR) downregulation and receptor uncoupling that are characteristic of end-stage human dilated cardiomyopathy, a process mediated in part by increased levels of beta-adrenergic receptor kinase (betaARK1). To explore whether chronic sustained NE stimulation is a primary stimulus that promotes deterioration in cardiac signaling, we characterized a gene-targeted mouse in which activation of the sympathetic nervous system cannot lead to an elevation in plasma NE and epinephrine. |
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| Keywords |
Adrenergic beta-Agonists/pharmacology; Animals; Cyclic AMP-Dependent Protein Kinases/metabolism; Dobutamine/pharmacology; Dopamine beta-Hydroxylase/genetics; Epinephrine/deficiency; Female; GTP-Binding Proteins/metabolism; Gene Targeting; Hemodynamics/drug effects; Hemodynamics/physiology; Male; Mice; Mice, Mutant Strains; Myocardial Contraction/drug effects; Myocardial Contraction/physiology; Norepinephrine/deficiency; Receptors, Adrenergic, beta/metabolism; Sarcolemma/metabolism; beta-Adrenergic Receptor Kinases |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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