Department of Optometry and Vision Science, Hadassah College, Jerusalem, Israel.
Channels (Austin). 2008 Mar-Apr;2(2):125-9. doi: 10.4161/chan.2.2.6026. Epub 2008 Mar 16.
The 30+ members of the family of TRP channels are diverse in their physiological roles, yet the mechanisms that regulate their gating may be conserved. In particular, all TRP channels show an activity-dependent inhibition which is mediated by Ca(2+). The mechanism by which Ca(2+) inhibits TRP channels is currently a matter of intense debate, with Ca(2+)-regulated kinases, phosphatases, phospholipases and calmodulin all proposed to be involved. In this review, we will discuss different mechanisms for Ca(2+)-dependent desensitization in TRP channels. We will conclude with a model that focuses on Ca(2+)-dependent activation of phospholipase C and Ca(2+) binding to calmodulin and propose that the phospholipase C and calmodulin pathways are structurally and functionally coupled.
TRP 通道家族的 30 多个成员在生理功能上具有多样性，但调节它们门控的机制可能是保守的。特别是，所有 TRP 通道都表现出一种活性依赖性抑制，这种抑制是由 Ca(2+)介导的。目前，Ca(2+)抑制 TRP 通道的机制是一个激烈争论的问题，Ca(2+)调节的激酶、磷酸酶、磷脂酶和钙调蛋白都被认为与之相关。在这篇综述中，我们将讨论 TRP 通道中 Ca(2+)依赖性脱敏的不同机制。我们将以一个专注于 PLC 依赖性 Ca(2+)激活和 Ca(2+)与钙调蛋白结合的模型作为结论，并提出 PLC 和钙调蛋白途径在结构和功能上是偶联的。
