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Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes.

Standard

Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes. / Rau, Thomas; Nose, Monika; Remmers, Ute; Weil, Joachim; Weissmüller, Astrid; Davia, Kerry; Harding, Sian; Peppel, Karsten; Koch, Walter J; Eschenhagen, Thomas.

in: FASEB J, Jahrgang 17, Nr. 3, 3, 2003, S. 523-525.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Rau, T, Nose, M, Remmers, U, Weil, J, Weissmüller, A, Davia, K, Harding, S, Peppel, K, Koch, WJ & Eschenhagen, T 2003, 'Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes.', FASEB J, Jg. 17, Nr. 3, 3, S. 523-525. <http://www.ncbi.nlm.nih.gov/pubmed/12631586?dopt=Citation>

APA

Rau, T., Nose, M., Remmers, U., Weil, J., Weissmüller, A., Davia, K., Harding, S., Peppel, K., Koch, W. J., & Eschenhagen, T. (2003). Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes. FASEB J, 17(3), 523-525. [3]. http://www.ncbi.nlm.nih.gov/pubmed/12631586?dopt=Citation

Vancouver

Rau T, Nose M, Remmers U, Weil J, Weissmüller A, Davia K et al. Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes. FASEB J. 2003;17(3):523-525. 3.

Bibtex

@article{36d78a35070d4edc9ba6e6c3ff2e33d9,
title = "Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes.",
abstract = "The role of Galpha(i)-2 overexpression in desensitization of beta-adrenergic signaling in heart failure is controversial. An adenovirus-based approach was used to investigate whether overexpression of Galpha(i)-2 impairs beta-adrenergic stimulation of adenylyl cyclase (AC) activity and cAMP levels in neonatal rat cardiac myocytes (NRCM) and cell shortening of adult rat ventricular myocytes (ARVM). Infection of NRCM with Ad5Galpha(i)-2 increased Galpha(i)-2 by 50-600% in a virus dose-dependent manner. Overexpression was paralleled by suppression of GTP- and isoprenaline-stimulated AC by 10-72% (P",
author = "Thomas Rau and Monika Nose and Ute Remmers and Joachim Weil and Astrid Weissm{\"u}ller and Kerry Davia and Sian Harding and Karsten Peppel and Koch, {Walter J} and Thomas Eschenhagen",
year = "2003",
language = "Deutsch",
volume = "17",
pages = "523--525",
journal = "FASEB J",
issn = "0892-6638",
publisher = "FASEB",
number = "3",

}

RIS

TY - JOUR

T1 - Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes.

AU - Rau, Thomas

AU - Nose, Monika

AU - Remmers, Ute

AU - Weil, Joachim

AU - Weissmüller, Astrid

AU - Davia, Kerry

AU - Harding, Sian

AU - Peppel, Karsten

AU - Koch, Walter J

AU - Eschenhagen, Thomas

PY - 2003

Y1 - 2003

N2 - The role of Galpha(i)-2 overexpression in desensitization of beta-adrenergic signaling in heart failure is controversial. An adenovirus-based approach was used to investigate whether overexpression of Galpha(i)-2 impairs beta-adrenergic stimulation of adenylyl cyclase (AC) activity and cAMP levels in neonatal rat cardiac myocytes (NRCM) and cell shortening of adult rat ventricular myocytes (ARVM). Infection of NRCM with Ad5Galpha(i)-2 increased Galpha(i)-2 by 50-600% in a virus dose-dependent manner. Overexpression was paralleled by suppression of GTP- and isoprenaline-stimulated AC by 10-72% (P

AB - The role of Galpha(i)-2 overexpression in desensitization of beta-adrenergic signaling in heart failure is controversial. An adenovirus-based approach was used to investigate whether overexpression of Galpha(i)-2 impairs beta-adrenergic stimulation of adenylyl cyclase (AC) activity and cAMP levels in neonatal rat cardiac myocytes (NRCM) and cell shortening of adult rat ventricular myocytes (ARVM). Infection of NRCM with Ad5Galpha(i)-2 increased Galpha(i)-2 by 50-600% in a virus dose-dependent manner. Overexpression was paralleled by suppression of GTP- and isoprenaline-stimulated AC by 10-72% (P

M3 - SCORING: Zeitschriftenaufsatz

VL - 17

SP - 523

EP - 525

JO - FASEB J

JF - FASEB J

SN - 0892-6638

IS - 3

M1 - 3

ER -