| First Author | Jenie RI | Year | 2013 |
| Journal | Genes Cells | Volume | 18 |
| Issue | 12 | Pages | 1095-106 |
| PubMed ID | 24134321 | Mgi Jnum | J:215736 |
| Mgi Id | MGI:5606154 | Doi | 10.1111/gtc.12099 |
| Citation | Jenie RI, et al. (2013) Increased ubiquitination and the crosstalk of G protein signaling in cardiac myocytes: involvement of Ric-8B in Gs suppression by Gq signal. Genes Cells 18(12):1095-106 |
| abstractText | Hyperactivation of Gq signaling causes cardiac hypertrophy, and beta-adrenergic receptor-mediated Gs signaling is attenuated in hypertrophic cardiomyocytes. Here, we found the increase in a global ubiquitination in hypertrophic mouse heart. The activation of Gq signaling resulted in the ubiquitination of Galphas in neonatal rat cardiomyocytes, reduced Galphas expression, and suppressed cAMP response to beta-adrenergic receptor stimulation. Ectopic expression of Galphaq induced a similar suppression, which is due to the degradation of Galphas by a ubiquitin-proteasome pathway. Co-expression of Ric-8B, a positive regulator of Galphas, effectively canceled the Galphaq-induced ubiquitination of Galphas and recovered the cAMP accumulation. In vitro, Galphaq competes for the binding of Galphas to Ric-8B. These data show a new role of Ric-8B in the crosstalk of two distinct G protein signaling pathways, which are possibly involved in a part of mechanisms of chronic heart failure. |
