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ygy19901025木蟲 (著名寫手)
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Abstract Glycogen synthase kinase-3 (GSK-3) plays a critical role in neuronal apoptosis. The two mammalian isoforms of the kinase, GSK-3α and GSK-3β, are inhibited by phosphorylation at Ser-21 and Ser-9, respectively. Depolarization, which is vital for neuronal survival, causes both an increase in Ser-21/9 phosphorylation and an inhibition of GSK-3α/β. 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. Using several approaches, we showed that both isoforms of GSK-3 are important for mediating neuronal apoptosis. 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. 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). CaMKII associated with and phosphorylated GSK-3α/β. Furthermore, the pro-survival effect of CaMKII was mediated by GSK-3 phosphorylation and inactivation. These findings identify a novel Ca(2+)/calmodulin/CaMKII/GSK-3 pathway that couples depolarization to neuronal survival. |
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wangyuan0929
金蟲 (小有名氣)
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【答案】應(yīng)助回帖
★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ...
RXMCDM: 金幣+3, 多謝應(yīng)助！ 2014-03-13 11:25:52
ygy19901025: 金幣+100, 翻譯EPI+1, ★★★★★最佳答案 2014-03-13 12:37:36
RXMCDM: 金幣+3, 多謝應(yīng)助！ 2014-03-13 11:25:52
ygy19901025: 金幣+100, 翻譯EPI+1, ★★★★★最佳答案 2014-03-13 12:37:36
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Abstract 摘要 Glycogen synthase kinase-3 (GSK-3) plays a critical role in neuronal apoptosis. 糖原合成酶激酶-3在神經(jīng)元凋亡中起到了關(guān)鍵作用。 The two mammalian isoforms of the kinase, GSK-3α and GSK-3β, are inhibited by phosphorylation at Ser-21 and Ser-9, respectively. 這一激酶在哺乳動物中的兩種同工酶（猜測，isoenzyme），GSK--3α和GSK-3β，會分別被Ser-21和Ser-9的磷酸化修飾所抑制。 Depolarization, which is vital for neuronal survival, causes both an increase in Ser-21/9 phosphorylation and an inhibition of GSK-3α/β. 對于神經(jīng)元的生存至關(guān)重要的去極化作用會導(dǎo)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磷酸化在依賴于去極化作用的神經(jīng)元生存中的作用，以及信號通路在去極化過程中對GSK-3磷酸化的作用在很大程度上還不得而知。 Using several approaches, we showed that both isoforms of GSK-3 are important for mediating neuronal apoptosis. 通過幾種新方法，我們發(fā)現(xiàn)GSK-3的兩個同工酶在介導(dǎo)神經(jīng)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突變體（S21A/S9A）促進(jìn)了凋亡，然而一個包圍了GSK-3β的Ser9的肽鏈則以一種依賴于磷酸化的方式對神經(jīng)元起到了保護(hù)作用；這些結(jié)果顯示，Ser-21/9的磷酸化在依賴于去極化作用的神經(jīng)元生存中起到了至關(guān)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). 我們發(fā)現(xiàn)GSK-3的Ser-21/9磷酸化是由依賴于鈣離子/鈣調(diào)蛋白的蛋白激酶II（CaMKII），而非Akt/PKB,PKA或者p90(RSK)所介導(dǎo)的。 CaMKII associated with and phosphorylated GSK-3α/β. CaMKII與磷酸化的GSK-3α/β相連（這個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的促存活效應(yīng)（pro-survival effect，也許有更貼切的術(shù)語）是由GSK-3磷酸化和失活所介導(dǎo)的。 These findings identify a novel Ca(2+)/calmodulin/CaMKII/GSK-3 pathway that couples depolarization to neuronal survival. 這些發(fā)現(xiàn)確定了一條新的鈣離子/鈣調(diào)蛋白/CaMKII/GSK-3途徑，這條途徑是與神經(jīng)元生存的去極化作用相偶聯(lián)的。 |
2樓2014-03-13 10:54:49
RXMCDM
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【答案】應(yīng)助回帖
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摘要 糖原合成酶激酶-3（GSK-3）對神經(jīng)細(xì)胞凋亡起著至關(guān)重要的作用。哺乳動物的兩種糖原合成酶激酶-3異構(gòu)體GSK-3α和GSK-3β通過Ser-21和Ser9磷酸化而被抑制。去極化對神經(jīng)元的存活至關(guān)重要，同時導(dǎo)致Ser-21和Ser9增加和GSK-3α和GSK-3β抑制。然而，GSK-3磷酸化在去極化依賴的神經(jīng)元存活的作用，以及信號轉(zhuǎn)導(dǎo)通路在去極化過程中促進(jìn)GSK-3磷酸化的作用仍然一無所知。 通過幾種方法，我們發(fā)現(xiàn)，GSK-3的兩個異構(gòu)體對介導(dǎo)神經(jīng)細(xì)胞凋亡都重要。 不能磷酸化的GSK-3α/β突變體（S21A/S9A）促進(jìn)細(xì)胞凋亡，而多肽包裹的GSK-3βSer-9 以磷酸化依賴的方式保護(hù)神經(jīng)元。這些結(jié)果表明 Ser-21/9磷酸化對去極化依賴的神經(jīng)元存活至關(guān)重要。我們的研究發(fā)現(xiàn)，GSK-3 Ser-21/9 磷酸化是由鈣（2 +）/鈣調(diào)蛋白依賴性蛋白激酶II（CaMKII）介導(dǎo)，Akt/ PKB、PKA以及 p90(RSK)都不介導(dǎo)。CaMKII與GSK-3α/β磷酸化相關(guān)。而且，CaMKII的的促神經(jīng)元存活作用由GSK-3的磷酸化失活介導(dǎo)。這些發(fā)現(xiàn)確認(rèn)了一種新的Ca（2+）/ calmodulin（鈣調(diào)節(jié)）/CaMKII/GSK-3通路，這一通路耦合到神經(jīng)元存活的去極化。 |
3樓2014-03-13 11:23:52
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