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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Nooh, Mohammed M. Bahouth, Suleiman W. Li, Xin |
| Description | Author Affiliation: Li X ( From the Department of Pharmacology, University of Tennessee Health Sciences Center, Memphis, Tennessee 38163.) |
| Abstract | Protein kinase A-anchoring proteins (AKAPs) participate in the formation of macromolecular signaling complexes that include protein kinases, ion channels, effector enzymes, and G-protein-coupled receptors. We examined the role of AKAP79/150 (AKAP5) in trafficking and signaling of the ß1-adrenergic receptor (ß1-AR). shRNA-mediated down-regulation of AKAP5 in HEK-293 cells inhibited the recycling of the ß1-AR. Recycling of the ß1-AR in AKAP5 knockdown cells was rescued by shRNA-resistant AKAP5. However, truncated mutants of AKAP5 with deletions in the domains involved in membrane targeting or in binding to calcineurin or PKA failed to restore the recycling of the ß1-AR, indicating that full-length AKAP5 was required. Furthermore, recycling of the ß1-AR in rat neonatal cardiac myocytes was dependent on targeting the AKAP5-PKA complex to the C-terminal tail of the ß1-AR. To analyze the role of AKAP5 more directly, recycling of the ß1-AR was determined in ventricular myocytes from AKAP5(-/-) mice. In AKAP5(-/-) myocytes, the agonist-internalized ß1-AR did not recycle, except when full-length AKAP5 was reintroduced. These data indicate that AKAP5 exerted specific and profound effects on ß1-AR recycling in mammalian cells. Biochemical or real time FRET-based imaging of cyclic AMP revealed that deletion of AKAP5 sensitized the cardiac ß1-AR signaling pathway to isoproterenol. Moreover, isoproterenol-mediated increase in contraction rate, surface area, or expression of ß-myosin heavy chains was significantly greater in AKAP5(-/-) myocytes than in AKAP5(+/+) myocytes. These results indicate a significant role for the AKAP5 scaffold in signaling and trafficking of the ß1-AR in cardiac myocytes and mammalian cells. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 47 |
| Volume Number | 288 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2013-11-22 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | A Kinase Anchor Proteins Metabolism Myocytes, Cardiac Receptors, Adrenergic, Beta-1 Signal Transduction Physiology Genetics Adrenergic Beta-1 Receptor Agonists Pharmacology Amino Acid Sequence Animals Cyclic AMP-Dependent Protein Kinases HEK293 Cells Isoproterenol Mice Mice, Knockout Cytology Myosin Heavy Chains Protein Transport Drug Effects Sequence Deletion Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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