|
|
【答案】应助回帖
★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ...
RXMCDM: 金币+3, 多谢应助！ 2014-03-13 11:25:52
ygy19901025: 金币+100, 翻译EPI+1, ★★★★★最佳答案 2014-03-13 12:37:36
Abstract
摘要
Glycogen synthase kinase-3 (GSK-3) plays a critical role in neuronal apoptosis.
糖原合成酶激酶-3在神经元凋亡中起到了关键作用。
The two mammalian isoforms of the kinase, GSK-3α and GSK-3β, are inhibited by phosphorylation at Ser-21 and Ser-9, respectively.
这一激酶在哺乳动物中的两种同工酶（猜测，isoenzyme），GSK--3α和GSK-3β，会分别被Ser-21和Ser-9的磷酸化修饰所抑制。
Depolarization, which is vital for neuronal survival, causes both an increase in Ser-21/9 phosphorylation and an inhibition of GSK-3α/β.
对于神经元的生存至关重要的去极化作用会导致Ser-21/9的磷酸化水平的上升，并抑制GSK-3α/β的活性。
However, the role of GSK-3 phosphorylation in depolarization-dependent neuron survival and the signaling pathway contributing to GSK-3 phosphorylation during depolarization remain largely unknown.
然而，GSK-3磷酸化在依赖于去极化作用的神经元生存中的作用，以及信号通路在去极化过程中对GSK-3磷酸化的作用在很大程度上还不得而知。
Using several approaches, we showed that both isoforms of GSK-3 are important for mediating neuronal apoptosis.
通过几种新方法，我们发现GSK-3的两个同工酶在介导神经元凋亡中起到了重要的作用。
Nonphosphorylatable GSK-3α/β mutants (S21A/S9A) promoted apoptosis, whereas a peptide encompassing Ser-9 of GSK-3β protected neurons in a phosphorylation-dependent manner; these results indicate a critical role for Ser-21/9 phosphorylation on depolarization-dependent neuron survival.
不可磷酸化的GSK-3α/β突变体（S21A/S9A）促进了凋亡，然而一个包围了GSK-3β的Ser9的肽链则以一种依赖于磷酸化的方式对神经元起到了保护作用；这些结果显示，Ser-21/9的磷酸化在依赖于去极化作用的神经元生存中起到了至关重要的作用。
We found that Ser-21/9 phosphorylation of GSK-3 was mediated by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) but not by Akt/PKB, PKA, or p90(RSK).
我们发现GSK-3的Ser-21/9磷酸化是由依赖于钙离子/钙调蛋白的蛋白激酶II（CaMKII），而非Akt/PKB,PKA或者p90(RSK)所介导的。
CaMKII associated with and phosphorylated GSK-3α/β.
CaMKII与磷酸化的GSK-3α/β相连（这个and是什么意思，存疑）。
Furthermore, the pro-survival effect of CaMKII was mediated by GSK-3 phosphorylation and inactivation.
此外，CaMKII的促存活效应（pro-survival effect，也许有更贴切的术语）是由GSK-3磷酸化和失活所介导的。
These findings identify a novel Ca(2+)/calmodulin/CaMKII/GSK-3 pathway that couples depolarization to neuronal survival.
这些发现确定了一条新的钙离子/钙调蛋白/CaMKII/GSK-3途径，这条途径是与神经元生存的去极化作用相偶联的。 |
|
回复此楼
一志愿北京科技材料科学与工程288分，求调剂
+14