S100A1: a regulator of striated muscle sarcoplasmic reticulum Ca2+ handling, sarcomeric, and mitochondrial function.
S100A1: a regulator of striated muscle sarcoplasmic reticulum Ca2+ handling, sarcomeric, and mitochondrial function.
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DOI：
10.1155/2010/178614
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发表时间：
2010
影响因子：
--
通讯作者：
Most P
中科院分区：
文献类型：
--
作者：
Völkers M;Rohde D;Goodman C;Most P
钙（Ca2+）信号传导在广泛的生理功能中起关键作用，包括控制心脏和骨骼肌的性能。为了确保细胞内Ca 2+振荡的时间和空间转导到下游信号网络和靶向操作的精确协调，肌肉组织中的Ca 2+循环调节由过多的不同分子进行。Ca2+ S100A1是Ca2+结合S100蛋白家族的成员，代表心肌和骨骼肌中最丰富的S100同种型。早期的研究揭示了S100A1在动物模型和人类健康和患病心脏组织中的不同表达模式。进一步的详细研究发现S100A1蛋白是横纹肌Ca2+处理完整性的基本要求。S100A1是心肌细胞Ca 2+循环和收缩性能的关键调节剂。S100A1介导的变力作用独立于β AR刺激的收缩性，并在βAR下游信号传导不变的情况下展开。 S100A1还在心脏肌节内的不同部位检测到，表明在肌丝功能中的潜在作用。最近，一项研究报告了S100A1在心肌细胞中的线粒体定位。此外，在动物心力衰竭模型中通过病毒心脏基因转移使S100A1蛋白水平正常化，导致心力衰竭进展中断并提高存活率。这篇简短的综述仅限于S100A1在心脏和骨骼肌Ca2+处理中的生理和病理生理相关性，特别关注其作为未来治疗干预的分子靶点的潜力。
Calcium (Ca2+) signaling plays a key role in a wide range of physiological functions including control of cardiac and skeletal muscle performance. To assure a precise coordination of both temporally and spatially transduction of intracellular Ca2+ oscillations to downstream signaling networks and target operations, Ca2+ cycling regulation in muscle tissue is conducted by a plethora of diverse molecules. Ca2+ S100A1 is a member of the Ca2+-binding S100 protein family and represents the most abundant S100 isoform in cardiac and skeletal muscle. Early studies revealed distinct expression patterns of S100A1 in healthy and diseased cardiac tissue from animal models and humans. Further elaborate investigations uncovered S100A1 protein as a basic requirement for striated muscle Ca2+ handling integrity. S100A1 is a critical regulator of cardiomyocyte Ca2+ cycling and contractile performance. S100A1-mediated inotropy unfolds independent and on top of βAR-stimulated contractility with unchanged βAR downstream signaling. S100A1 has further been detected at different sites within the cardiac sarcomere indicating potential roles in myofilament function. More recently, a study reported a mitochondrial location of S100A1 in cardiomyocytes. Additionally, normalizing the level of S100A1 protein by means of viral cardiac gene transfer in animal heart failure models resulted in a disrupted progression towards cardiac failure and enhanced survival. This brief review is confined to the physiological and pathophysiological relevance of S100A1 in cardiac and skeletal muscle Ca2+ handling with a particular focus on its potential as a molecular target for future therapeutic interventions.
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影响因子：
64.8
作者：
Heierhorst, J;Kobe, B;Kemp, BE
通讯作者：
Kemp, BE
影响因子：
5.5
作者：
Hernandez-Ochoa, Erick O.;Prosser, Benjamin L.;Schneider, Martin F.
通讯作者：
Schneider, Martin F.
影响因子：
4.8
作者：
Most, P;Remppis, A;Koch, WJ
通讯作者：
Koch, WJ
影响因子：
4.8
作者：
Most, P;Boerries, M;Remppis, A
通讯作者：
Remppis, A
DOI：
10.1111/j.1432-1033.1996.454rr.x
发表时间：
1996-12-15
期刊：
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子：
--
作者：
Heierhorst, J;Tang, XX;Benian, GM
通讯作者：
Benian, GM