 |
 |
 |
 |
 |
 |
||
 |
 |
 |
 |
 |
| 3 | 1/1 | 返回列表 |
| 查看: 567 | 回復(fù): 2 | ||
| 本帖產(chǎn)生 1 個(gè) 翻譯EPI ，點(diǎn)擊這里進(jìn)行查看 | ||
ygy19901025木蟲 (著名寫手)
|
[求助]
生物類摘要，求翻譯英譯漢，金幣奉上
|
|
|
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. |
回復(fù)此樓» 猜你喜歡
生物學(xué)學(xué)碩求調(diào)劑
已經(jīng)有10人回復(fù)
-
上海電力大學(xué)材料防護(hù)與新材料重點(diǎn)實(shí)驗(yàn)室招收調(diào)劑研究生（材料、化學(xué)、電化學(xué)，環(huán)境）
已經(jīng)有4人回復(fù)
-
材料學(xué)求調(diào)劑
已經(jīng)有6人回復(fù)
-
303求調(diào)劑
已經(jīng)有5人回復(fù)
-
一志愿武理085500機(jī)械專業(yè)總分300求調(diào)劑
已經(jīng)有7人回復(fù)
-
考研調(diào)劑
已經(jīng)有4人回復(fù)
-
281求調(diào)劑
已經(jīng)有4人回復(fù)
-
0805 316求調(diào)劑
已經(jīng)有6人回復(fù)
-
085601求調(diào)劑總分293英一數(shù)二
已經(jīng)有3人回復(fù)
-
08工學(xué)調(diào)劑
已經(jīng)有17人回復(fù)
ygy19901025
木蟲 (著名寫手)
- 應(yīng)助: 24 (小學(xué)生)
- 金幣: 1298.3
- 散金: 1690
- 紅花: 9
- 沙發(fā): 7
- 帖子: 2956
- 在線: 106.7小時(shí)
- 蟲號: 2614551
- 注冊: 2013-08-24
- 專業(yè): 神經(jīng)生物學(xué)
怎么沒人回復(fù)呢 2樓2014-03-13 12:40:31
wangyuan0929
金蟲 (小有名氣)
- 翻譯EPI: 12
- 應(yīng)助: 10 (幼兒園)
- 金幣: 706.2
- 紅花: 8
- 帖子: 88
- 在線: 21.6小時(shí)
- 蟲號: 2233248
- 注冊: 2013-01-10
- 專業(yè): 環(huán)境微生物學(xué)
【答案】應(yīng)助回帖
★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ...
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
|
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
相關(guān)版塊跳轉(zhuǎn)
我要訂閱樓主 ygy19901025 的主題更新
| 3 | 1/1 | 返回列表 |
| 最具人氣熱帖推薦 [查看全部] | 作者 | 回/看 | 最后發(fā)表 | |
|---|---|---|---|---|
|
[考研] 上海電力大學(xué)材料防護(hù)與新材料重點(diǎn)實(shí)驗(yàn)室招收調(diào)劑研究生（材料、化學(xué)、電化學(xué)，環(huán)境） +4 | 我愛學(xué)電池 2026-03-23 | 4/200 |
|
|---|---|---|---|---|
|
[考研] 調(diào)劑 +4 | 13853210211 2026-03-24 | 4/200 |
|
|
|
[考研] 291求調(diào)劑 +3 | HanBeiNingZC 2026-03-24 | 3/150 |
|
|
|
[考研] 【雙一流院校新能源、環(huán)境材料，材料加工與模擬招收大量調(diào)劑】 +4 | Higraduate 2026-03-22 | 7/350 |
|
|
|
[考研] 求材料，環(huán)境專業(yè)調(diào)劑 +3 | 18567500178 2026-03-18 | 3/150 |
|
|
|
[考研] 284求調(diào)劑 +3 | yanzhixue111 2026-03-23 | 6/300 |
|
|
|
[考研] 070300，一志愿北航320求調(diào)劑 +3 | Jerry0216 2026-03-22 | 5/250 |
|
|
|
[考研] 323求調(diào)劑 +6 | 洼小桶 2026-03-18 | 6/300 |
|
|
|
[考研]
 一志愿東華大學(xué)化學(xué)070300，求調(diào)劑
+7
|
2117205181 2026-03-21 | 8/400 |
|
|
|
[考研] 324求調(diào)劑 +6 | lucky呀呀呀鴨 2026-03-20 | 6/300 |
|
|
|
[考研] 生物學(xué)調(diào)劑 +5 | Surekei 2026-03-21 | 5/250 |
|
|
|
[考研] 318求調(diào)劑 +4 | plum李子 2026-03-21 | 7/350 |
|
|
|
[考研] 材料學(xué)碩301分求調(diào)劑 +7 | Liyouyumairs 2026-03-21 | 7/350 |
|
|
|
[考研] 求調(diào)劑 +3 | 13341 2026-03-20 | 3/150 |
|
|
|
[考研] 材料 271求調(diào)劑 +5 | 展信悅_ 2026-03-21 | 5/250 |
|
|
|
[考研] 265求調(diào)劑 +12 | 梁梁校校 2026-03-19 | 14/700 |
|
|
|
[考研] A區(qū)線材料學(xué)調(diào)劑 +5 | 周周無極 2026-03-20 | 5/250 |
|
|
|
[考研] 一志愿吉林大學(xué)材料學(xué)碩321求調(diào)劑 +11 | Ymlll 2026-03-18 | 15/750 |
|
|
|
[考研] 086500 325 求調(diào)劑 +3 | 領(lǐng)帶小熊 2026-03-19 | 3/150 |
|
|
|
[考研] 085410人工智能專碩317求調(diào)劑（0854都可以） +4 | xbxudjdn 2026-03-18 | 4/200 |
|