dc.contributor.author |
Tóth, András |
|
dc.contributor.author |
Gyombolai, Pál |
|
dc.contributor.author |
Szalai, Bence |
|
dc.contributor.author |
Várnai, Péter |
|
dc.contributor.author |
Turu, Gábor |
|
dc.contributor.author |
Hunyady, László |
|
dc.date.accessioned |
2017-06-19T08:53:12Z |
|
dc.date.available |
2017-06-19T08:53:12Z |
|
dc.date.issued |
2017 |
|
dc.identifier |
85007399602 |
|
dc.identifier.citation |
pagination=113-124;
journalVolume=442;
journalTitle=MOLECULAR AND CELLULAR ENDOCRINOLOGY; |
|
dc.identifier.uri |
http://repo.lib.semmelweis.hu//handle/123456789/4099 |
|
dc.identifier.uri |
doi:10.1016/j.mce.2016.11.027 |
|
dc.description.abstract |
Heterodimerization between angiotensin type 1A receptor (AT1R) and β2-adrenergic receptor (β2AR) has been shown to modulate G protein-mediated effects of these receptors. Activation of G protein-coupled receptors (GPCRs) leads to β-arrestin binding, desensitization, internalization and G protein-independent signaling of GPCRs. Our aim was to study the effect of heterodimerization on β-arrestin coupling. We found that β-arrestin binding of β2AR is affected by activation of AT1Rs. Costimulation with angiotensin II and isoproterenol markedly enhanced the interaction between β2AR and β-arrestins, by prolonging the lifespan of β2AR-induced β-arrestin2 clusters at the plasma membrane. While candesartan, a conventional AT1R antagonist, had no effect on the β-arrestin2 binding to β2AR, TRV120023, a β-arrestin biased agonist, enhanced the interaction. These findings reveal a new crosstalk mechanism between AT1R and β2AR, and suggest that enhanced β-arrestin2 binding to β2AR can contribute to the pharmacological effects of biased AT1R agonists. © 2016 |
|
dc.relation.ispartof |
urn:issn:0303-7207 |
|
dc.title |
Angiotensin type 1A receptor regulates β-arrestin binding of the β2-adrenergic receptor via heterodimerization |
|
dc.type |
Journal Article |
|
dc.date.updated |
2017-02-15T09:34:18Z |
|
dc.language.rfc3066 |
en |
|
dc.identifier.mtmt |
3171969 |
|
dc.contributor.department |
SE/AOK/I/Élettani Intézet |
|
dc.contributor.department |
SE/AOK/I/ÉI/MTA-SE Molekuláris Élettani Kutatócsoport |
|
dc.contributor.institution |
Semmelweis Egyetem |
|
dc.mtmt.swordnote |
FELTÖLTŐ: Sonnevend Kinga - sonnevend.kinga@med.semmelweis-univ.hu |
|