The inotropic peptide ?ARKct improves ?AR responsiveness in normal and failing cardiomyocytes through G(??)-mediated L-type calcium current disinhibition

Völkers, Mirko; Weidenhammer, Christian; Herzog, Nicole; Qiu, Gang; Spaich, Kristin; von Wegner, Frederic; Peppel, Karsten; Müller, Oliver J; Schinkel, Stefanie; Rabinowitz, Joseph E; Hippe, Hans-Jörg; Brinks, Henriette; Katus, Hugo A; Koch, Walter J; Eckhart, Andrea D; Friedrich, Oliver; Most, Patrick (2011). The inotropic peptide ?ARKct improves ?AR responsiveness in normal and failing cardiomyocytes through G(??)-mediated L-type calcium current disinhibition. Circulation research, 108(1), pp. 27-39. Baltimore, Md.: Lippincott Williams & Wilkins 10.1161/CIRCRESAHA.110.225201

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The G(βγ)-sequestering peptide β-adrenergic receptor kinase (βARK)ct derived from the G-protein-coupled receptor kinase (GRK)2 carboxyl terminus has emerged as a promising target for gene-based heart failure therapy. Enhanced downstream cAMP signaling has been proposed as the underlying mechanism for increased β-adrenergic receptor (βAR) responsiveness. However, molecular targets mediating improved cardiac contractile performance by βARKct and its impact on G(βγ)-mediated signaling have yet to be fully elucidated.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Cardiovascular Disorders (DHGE) > Clinic of Heart Surgery

UniBE Contributor:

Most, Henriette

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0009-7330

Publisher:

Lippincott Williams & Wilkins

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:13

Last Modified:

27 Feb 2024 14:29

Publisher DOI:

10.1161/CIRCRESAHA.110.225201

PubMed ID:

21106943

Web of Science ID:

000285965500008

URI:

https://boris.unibe.ch/id/eprint/2747 (FactScience: 205621)

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