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ygy19901025木蟲 (著名寫手)
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[求助]
生物類摘要，求翻譯英譯漢，金幣奉上
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Abstract Glycogen synthase kinase-3β (GSK-3β), a key regulator of neuronal apoptosis, is inhibited by the phosphorylation of Ser-9/Ser-389 and was recently shown to be cleaved by calpain at the N terminus, leading to its subsequent activation. In this study calpain was found to cleave GSK-3β not only at the N terminus but also at the C terminus, and cleavage sites were identified at residues Thr-38–Thr-39 and Ile-384–Gln-385. Furthermore, the cleavage of GSK-3β occurred in tandem with Ser-9 dephosphorylation during cerebellar granule neuron apoptosis. Increasing Ser-9 phosphorylation of GSK-3β by inhibiting phosphatase 1/2A or pretreating with purified active Akt inhibited calpain-mediated cleavage of GSK-3β at both N and C termini, whereas non-phosphorylatable mutant GSK-3β S9A facilitated its cleavage. In contrast, Ser-389 phosphorylation selectively inhibited the cleavage of GSK-3β at the C terminus but not the N terminus. Calpain-mediated cleavage resulted in three truncated products, all of which contained an intact kinase domain: ΔN-GSK-3β (amino acids 39–420), ΔC-GSK-3β (amino acids 1–384), and ΔN/ΔC-GSK-3β (amino acids 39–384). All three truncated products showed increased kinase and pro-apoptotic activity, with ΔN/ΔC-GSK-3β being the most active form. This observation suggests that the GSK-3β C terminus acts as an autoinhibitory domain similar to the N terminus. Taken together, these findings demonstrate that calpain-mediated cleavage activates GSK-3β by removing its N- and C-terminal autoinhibitory domains and that Ser-9 phosphorylation inhibits the cleavage of GSK-3β at both termini. In contrast, Ser-389 phosphorylation inhibits only C-terminal cleavage but not N-terminal cleavage. These findings also identify a mechanism by which site-specific phosphorylation and calpain-mediated cleavage operate in concert to regulate GSK-3β activity. |
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wangyuan0929
金蟲 (小有名氣)
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【答案】應(yīng)助回帖
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ygy19901025: 金幣+100, 翻譯EPI+1, ★★★★★最佳答案 2014-03-13 22:11:24
ygy19901025: 金幣+100, 翻譯EPI+1, ★★★★★最佳答案 2014-03-13 22:11:24
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Abstract 摘要 Glycogen synthase kinase-3β (GSK-3β), a key regulator of neuronal apoptosis, is inhibited by the phosphorylation of Ser-9/Ser-389 and was recently shown to be cleaved by calpain at the N terminus, leading to its subsequent activation. 糖原合成酶激酶-3β（GSK-3β），是神經(jīng)元凋亡的關(guān)鍵調(diào)控物質(zhì)，會(huì)受到Ser-9/Ser-389位點(diǎn)磷酸化的抑制，最近發(fā)現(xiàn)它可以被鈣蛋白酶在N端切斷，這一反應(yīng)隨后將其活化。 In this study calpain was found to cleave GSK-3β not only at the N terminus but also at the C terminus, and cleavage sites were identified at residues Thr-38–Thr-39 and Ile-384–Gln-385. 本研究中發(fā)現(xiàn)鈣蛋白酶不僅能切斷GSK-3β的N端，還可以切開其C末端，并確定了其酶切位點(diǎn)為Thr-38/Thr-39和Ile-384/Gln-385這兩對(duì)氨基酸殘基之間。 Furthermore, the cleavage of GSK-3β occurred in tandem with Ser-9 dephosphorylation during cerebellar granule neuron apoptosis. 另外，GSK-3β的切斷是與Ser-9的去磷酸化過程一起，在小腦顆粒神經(jīng)元凋亡過程中發(fā)生的。 Increasing Ser-9 phosphorylation of GSK-3β by inhibiting phosphatase 1/2A or pretreating with purified active Akt inhibited calpain-mediated cleavage of GSK-3β at both N and C termini, whereas non-phosphorylatable mutant GSK-3β S9A facilitated its cleavage. 通過抑制磷酸酶1/2A或用純化過的活化態(tài)的Akt進(jìn)行預(yù)處理，來提高Ser-9的磷酸化程度，可以抑制鈣蛋白酶介導(dǎo)的GSK-3β在N末端和C末端發(fā)生的斷裂，然而不可磷酸化的GSK-3β突變體S9A則能夠促進(jìn)其斷裂。 In contrast, Ser-389 phosphorylation selectively inhibited the cleavage of GSK-3β at the C terminus but not the N terminus. 相比之下，Ser-389的磷酸化選擇性的抑制了GSK-3β在C末端的斷裂，而對(duì)N末端沒有影響。 Calpain-mediated cleavage resulted in three truncated products, all of which contained an intact kinase domain: ΔN-GSK-3β (amino acids 39–420), ΔC-GSK-3β (amino acids 1–384), and ΔN/ΔC-GSK-3β (amino acids 39–384). 鈣蛋白酶介導(dǎo)的斷裂產(chǎn)生了三種酶切產(chǎn)物，它們都包含了完整的激酶結(jié)構(gòu)域：ΔN-GSK-3β (氨基酸殘基39–420), ΔC-GSK-3β (氨基酸殘基1–384), 以及ΔN/ΔC-GSK-3β (氨基酸殘基39–384). All three truncated products showed increased kinase and pro-apoptotic activity, with ΔN/ΔC-GSK-3β being the most active form. 所有這三種酶切產(chǎn)物顯示出了更高的激酶活性以及促凋亡活性，其中 ΔN/ΔC-GSK-3β 活性最高。 This observation suggests that the GSK-3β C terminus acts as an autoinhibitory domain similar to the N terminus. 這一現(xiàn)象顯示出GSK-3β的C末端與N末端類似，都是一種起自我抑制作用的結(jié)構(gòu)域。 Taken together, these findings demonstrate that calpain-mediated cleavage activates GSK-3β by removing its N- and C-terminal autoinhibitory domains and that Ser-9 phosphorylation inhibits the cleavage of GSK-3β at both termini. 綜上所述，這些發(fā)現(xiàn)顯示出：鈣蛋白酶介導(dǎo)的斷裂移除了N末端和C末端的自我抑制結(jié)構(gòu)域，從而活化了GSK-3β，Ser-9的磷酸化作用抑制了GSK-3β的兩個(gè)末端發(fā)生的斷裂反應(yīng)。 In contrast, Ser-389 phosphorylation inhibits only C-terminal cleavage but not N-terminal cleavage. 相比之下，Ser-389的磷酸化只能一直C末端的斷裂，而不抑制N末端斷裂。 These findings also identify a mechanism by which site-specific phosphorylation and calpain-mediated cleavage operate in concert to regulate GSK-3β activity. 這些發(fā)現(xiàn)還確定了一個(gè)位點(diǎn)特異性磷酸化作用和鈣蛋白酶介導(dǎo)的斷裂作用一齊調(diào)節(jié)GSK-3β的活性的作用機(jī)制。 |
3樓2014-03-13 14:48:38
ygy19901025
木蟲 (著名寫手)
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怎么沒人回復(fù)呢 2樓2014-03-13 12:40:31
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