Neuronal STIMulation at rest.

Neuronal STIMulation at rest.
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DOI:
10.1126/scisignal.2005556
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发表时间:
2014-07-22
期刊:
影响因子:
7.3
通讯作者:
Soboloff J
Soboloff J
中科院分区:
生物学1区
文献类型:
--
作者:
Hooper R;Rothberg BS;Soboloff J

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自第一个STIM和后来的奥赖以来,近十年过去了,蛋白质被鉴定为钙库操纵的钙进入(SOCE)的分子成分。尽管它们在免疫功能中的作用已被深入研究,但STIM和奥赖在神经元细胞中的作用却不太清楚。Lalonde等人表明,当神经元超极化或“静止”时,组成性内质网(ER)Ca2+释放导致SOCE介导的神经元转录因子激活。确切地说,为什么ER Ca 2+释放是神经元中的组成性的仍然是一个重要的问题。不管答案如何,这一观察结果提供了一个有趣的新视角,说明为什么相对低丰度,小电导通道(如Orai1)在神经元中很重要,神经元中含有相对丰富的电压操纵的Ca2+通道。
Almost a decade has passed since first STIM, and later Orai, proteins were identified as the molecular constituents of store-operated calcium entry (SOCE). Whereas their roles in immune function have been intensely investigated, the roles of STIM and Orai in neuronal cells have been much less clear. Lalonde et al. show that when neurons are hyperpolarized or “at rest”, constitutive endoplasmic reticulum (ER) Ca2+ release leads to SOCE-mediated activation of neuronal transcription factors. Precisely why ER Ca2+ release is constitutive in neurons remains an important question. Irrespective of the answer, this observation provides an intriguing new perspective into why a relatively low-abundance, small-conductance channel such as Orai1 would be important in neurons, which contain a relative abundance of voltage-operated Ca2+ channels.
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