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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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ygy19901025
木蟲 (著名寫手)
- 應助: 24 (小學生)
- 金幣: 1298.3
- 散金: 1690
- 紅花: 9
- 沙發(fā): 7
- 帖子: 2956
- 在線: 106.7小時
- 蟲號: 2614551
- 注冊: 2013-08-24
- 專業(yè): 神經生物學
怎么沒人回復呢 2樓2014-03-13 12:40:31
wangyuan0929
金蟲 (小有名氣)
- 翻譯EPI: 12
- 應助: 10 (幼兒園)
- 金幣: 706.2
- 紅花: 8
- 帖子: 88
- 在線: 21.6小時
- 蟲號: 2233248
- 注冊: 2013-01-10
- 專業(yè): 環(huán)境微生物學
【答案】應助回帖
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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），是神經元凋亡的關鍵調控物質，會受到Ser-9/Ser-389位點磷酸化的抑制，最近發(fā)現它可以被鈣蛋白酶在N端切斷，這一反應隨后將其活化。 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為Thr-38/Thr-39和Ile-384/Gln-385這兩對氨基酸殘基之間。 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進行預處理，來提高Ser-9的磷酸化程度，可以抑制鈣蛋白酶介導的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). 鈣蛋白酶介導的斷裂產生了三種酶切產物，它們都包含了完整的激酶結構域：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構域。 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)現顯示出：鈣蛋白酶介導的斷裂移除了N末端和C末端的自我抑制結構域，從而活化了GSK-3β，Ser-9的磷酸化作用抑制了GSK-3β的兩個末端發(fā)生的斷裂反應。 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)現還確定了一個位點特異性磷酸化作用和鈣蛋白酶介導的斷裂作用一齊調節(jié)GSK-3β的活性的作用機制。 |
3樓2014-03-13 14:48:38
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