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Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling.

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Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling. / Wittköpper, Katrin; Dobrev, Dobromir; Eschenhagen, Thomas; El-Armouche, Ali.

In: CARDIOVASC RES, Vol. 91, No. 3, 3, 2011, p. 392-401.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wittköpper, K, Dobrev, D, Eschenhagen, T & El-Armouche, A 2011, 'Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling.', CARDIOVASC RES, vol. 91, no. 3, 3, pp. 392-401. <http://www.ncbi.nlm.nih.gov/pubmed/21354993?dopt=Citation>

APA

Wittköpper, K., Dobrev, D., Eschenhagen, T., & El-Armouche, A. (2011). Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling. CARDIOVASC RES, 91(3), 392-401. [3]. http://www.ncbi.nlm.nih.gov/pubmed/21354993?dopt=Citation

Vancouver

Wittköpper K, Dobrev D, Eschenhagen T, El-Armouche A. Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling. CARDIOVASC RES. 2011;91(3):392-401. 3.

Bibtex

@article{722cdf7908ab48b382b8c3686989dc8b,
title = "Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling.",
abstract = "Control of protein phosphorylation/dephosphorylation events occurs through regulation of protein kinases and phosphatases. The phosphatase type 1 (PP-1) compromises the main activity of Ser/Thr protein phosphatases in the heart. Inhibitor-1 (I-1) was the first endogenous molecule found to specifically inhibit PP-1. Notably, I-1 is activated by cAMP-dependent protein kinase A (PKA) and the subsequent prevention of target-dephosphorylation by PP-1 provides distal amplification of -adrenoceptor ( -AR) signaling. I-1 was found to be downregulated and hypophosphorylated in human and experimental heart failure but hyperactive in human atrial fibrillation, implicating I-1 in the pathogenesis of heart failure and arrhythmias. Consequently, the therapeutic potential of I-1 in heart failure and arrhythmias has been recently addressed by the generation and analysis of several I-1 genetic mouse models. This review summarizes and discusses these data, highlights partially controversial issues on whether I-1 should be therapeutically reinforced or inhibited and suggests future directions to better understand the functional role of I-1 in physiological and pathological -AR signaling.",
author = "Katrin Wittk{\"o}pper and Dobromir Dobrev and Thomas Eschenhagen and Ali El-Armouche",
year = "2011",
language = "Deutsch",
volume = "91",
pages = "392--401",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Phosphatase-1-inhibitor-1 in physiological and pathological {beta}-adrenoceptor signaling.

AU - Wittköpper, Katrin

AU - Dobrev, Dobromir

AU - Eschenhagen, Thomas

AU - El-Armouche, Ali

PY - 2011

Y1 - 2011

N2 - Control of protein phosphorylation/dephosphorylation events occurs through regulation of protein kinases and phosphatases. The phosphatase type 1 (PP-1) compromises the main activity of Ser/Thr protein phosphatases in the heart. Inhibitor-1 (I-1) was the first endogenous molecule found to specifically inhibit PP-1. Notably, I-1 is activated by cAMP-dependent protein kinase A (PKA) and the subsequent prevention of target-dephosphorylation by PP-1 provides distal amplification of -adrenoceptor ( -AR) signaling. I-1 was found to be downregulated and hypophosphorylated in human and experimental heart failure but hyperactive in human atrial fibrillation, implicating I-1 in the pathogenesis of heart failure and arrhythmias. Consequently, the therapeutic potential of I-1 in heart failure and arrhythmias has been recently addressed by the generation and analysis of several I-1 genetic mouse models. This review summarizes and discusses these data, highlights partially controversial issues on whether I-1 should be therapeutically reinforced or inhibited and suggests future directions to better understand the functional role of I-1 in physiological and pathological -AR signaling.

AB - Control of protein phosphorylation/dephosphorylation events occurs through regulation of protein kinases and phosphatases. The phosphatase type 1 (PP-1) compromises the main activity of Ser/Thr protein phosphatases in the heart. Inhibitor-1 (I-1) was the first endogenous molecule found to specifically inhibit PP-1. Notably, I-1 is activated by cAMP-dependent protein kinase A (PKA) and the subsequent prevention of target-dephosphorylation by PP-1 provides distal amplification of -adrenoceptor ( -AR) signaling. I-1 was found to be downregulated and hypophosphorylated in human and experimental heart failure but hyperactive in human atrial fibrillation, implicating I-1 in the pathogenesis of heart failure and arrhythmias. Consequently, the therapeutic potential of I-1 in heart failure and arrhythmias has been recently addressed by the generation and analysis of several I-1 genetic mouse models. This review summarizes and discusses these data, highlights partially controversial issues on whether I-1 should be therapeutically reinforced or inhibited and suggests future directions to better understand the functional role of I-1 in physiological and pathological -AR signaling.

M3 - SCORING: Zeitschriftenaufsatz

VL - 91

SP - 392

EP - 401

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 3

M1 - 3

ER -