Redox regulation of RyR-mediated Ca2+ release in muscle and neurons
Redox regulation of RyR-mediated Ca2+ release in muscle and neurons
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DOI：
10.4067/s0716-97602004000400007
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发表时间：
2004-01-01
影响因子：
6.7
通讯作者：
DONOSO, PAULINA
中科院分区：
文献类型：
--
作者：
HIDALGO, CECILIA;BULL, RICARDO;DONOSO, PAULINA
骨骼肌和心肌或大脑皮层神经元的细胞内兰尼碱受体/Ca 2+释放通道的氧化还原状态的变化影响其活性。特别地，氧化或烷基化通道蛋白的游离SH残基的试剂强烈增强Ca 2+诱导的Ca 2+释放，而还原剂具有相反的作用。我们将在这里讨论如何修改高活性的半胱氨酸残基的内源性氧化还原剂或细胞的氧化还原状态的影响RyR通道激活的Ca 2+和ATP或抑制Mg 2+。这些结果对细胞Ca 2+信号传导可能的生理和病理影响也将得到解决。
Changes in the redox state of the intracellular ryanodine receptor/Ca2+ release channels of skeletal and cardiac muscle or brain cortex neurons affect their activity. In particular, agents that oxidize or alkylate free SH residues of the channel protein strongly enhance Ca2+-induced Ca2+ release, whereas reducing agents have the opposite effects. We will discuss here how modifications of highly reactive cysteine residues by endogenous redox agents or cellular redox state influence RyR channel activation by Ca2+ and ATP or inhibition by Mg2+. Possible physiological and pathological implications of these results on cellular Ca2+ signaling will be addressed as well.