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ygy19901025木蟲(chóng) (著名寫(xiě)手)
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Abstract The proapoptotic BH3-only protein Bim is a crucial regulator of neuronal apoptosis. Previous studies have indicated the involvement of the c-Jun, FOXO1/3a, and B/C-Myb transcription factors in the regulation of Bim during neuronal apoptosis. However, the mechanism underlying the transcriptional regulation of Bim in activity deprivation-induced neuronal apoptosis has remained unclear. The present study demonstrates that early growth response 1 (Egr-1), rather than c-Jun, FOXO1/3a, or B/C-Myb, directly transactivates Bim gene expression to mediate apoptosis of rat cerebellar granule neurons. We showed that Egr-1 was sufficient and necessary for neuronal apoptosis. Suppression of Egr-1 activity using dominant-negative mutant or knockdown of Egr-1 using small interfering RNAs led to a decrease in Bim expression, whereas overexpression of Egr-1 resulted in induction of Bim. Deletion and site-directed mutagenesis of the Bim promoter revealed that Bim transcriptional activation depends primarily on a putative Egr-binding sequence between nucleotides -56 and -47 upstream of the start site. We also showed that Egr-1 binding to this sequence increased in response to activity deprivation in vitro and in vivo. Moreover, inhibition of Egr-1 binding to the Bim promoter, by mithramycin A and chromomycin A3, reduced the activity deprivation-induced increases in Bim promoter activity and mRNA and protein levels and protected neurons from apoptosis, further supporting the Egr-1-mediated transactivation of Bim. Additionally, Bim overcame the Egr-1 knockdown-mediated inhibition ofapoptosis, whereas Bim knockdown impaired the increase in apoptosis induced by Egr-1. These findings establish Bim as an Egr-1 target gene in neurons, uncovering a novel Egr-1/Bim pathway by which activity deprivation induces neuronal apoptosis. |
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★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ...
RXMCDM: 金幣+2, 多謝應(yīng)助，用不著一上來(lái)就翻這么長(zhǎng)的吧！ 2014-03-12 22:02:48
ygy19901025: 金幣+100, 翻譯EPI+1, ★★★★★最佳答案 2014-03-12 23:49:40
RXMCDM: 金幣+2, 多謝應(yīng)助，用不著一上來(lái)就翻這么長(zhǎng)的吧！ 2014-03-12 22:02:48
ygy19901025: 金幣+100, 翻譯EPI+1, ★★★★★最佳答案 2014-03-12 23:49:40
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促凋亡的BH3-only蛋白質(zhì)Bim是神經(jīng)元凋亡的重要調(diào)節(jié)器。先前的研究已經(jīng)表明c-Jun,FOXO1/3a,B / C-Myb三種轉(zhuǎn)錄因子參與了Bim在神經(jīng)元凋亡過(guò)程中的調(diào)節(jié)。然而,Bim在誘發(fā)型活性缺失的神經(jīng)元凋亡過(guò)程中的潛在轉(zhuǎn)錄調(diào)控機(jī)制仍然不清楚。目前的研究表明，是早期生長(zhǎng)反應(yīng)基因(Egr-1),而不是c-Jun FOXO1/3a,或B / C-Myb直接轉(zhuǎn)錄Bim基因并使其表達(dá)以調(diào)節(jié)大鼠小腦顆粒神經(jīng)元的凋亡。我們發(fā)現(xiàn),Egr-1對(duì)神經(jīng)元凋亡是充分必要的。利用顯性負(fù)性突變體抑制Egr-1活性或利用小分子干擾的RNAs使Egr-1基因沉默，會(huì)導(dǎo)致Bim表達(dá)減少,反之超表達(dá)的Egr-1就會(huì)使Bim表達(dá)增加。Bim缺失和Bim定向誘變啟動(dòng)子都表明,Bim轉(zhuǎn)錄激活主要依賴一個(gè)假定存在于起始位置上游核苷酸-56與-47之間的Egr結(jié)合序列。我們還發(fā)現(xiàn),這種Egr-1的結(jié)合序列會(huì)使得體內(nèi)外Bim活性損失增加。此外,通過(guò)光神霉素和色霉素A3抑制Egr-1結(jié)合Bim啟動(dòng)子,減少了誘發(fā)型活性缺失從而增加Bim的活性，增加mRNA數(shù)量，提高蛋白質(zhì)水平，防止神經(jīng)元凋亡,進(jìn)一步增強(qiáng)Egr-1對(duì)Bim轉(zhuǎn)錄的調(diào)節(jié)。此外,Bim overcame the Egr-1 knockdown-mediated inhibition ofapoptosis（這句實(shí)在不會(huì)）,而B(niǎo)im 基因沉默削弱了Egr-1引起的細(xì)胞凋亡增加。這些發(fā)現(xiàn)證實(shí)了Bim是Egr-1在神經(jīng)元中的靶基因,并揭示了Egr-1 / Bim活性不足導(dǎo)致神經(jīng)元凋亡的新途徑。 PS：由于譯者水平有限且對(duì)生物學(xué)了解不足，有些地方翻譯得還不到位，故此文只能作為參考，還望諒解。 |
2樓2014-03-12 21:57:16
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RXMCDM: 建議你不要亂翻！ 2014-03-12 22:56:58
| 的proapoptotic BH3-only蛋白質(zhì)Bim是神經(jīng)元凋亡的重要調(diào)節(jié)器。先前的研究已經(jīng)表明c-Jun的參與,FOXO1/3a,B / C-Myb轉(zhuǎn)錄因子在Bim在神經(jīng)元凋亡的調(diào)節(jié)。然而,潛在的轉(zhuǎn)錄調(diào)控機(jī)制Bim活動(dòng)deprivation-induced神經(jīng)元凋亡仍然不清楚。目前的研究表明早期生長(zhǎng)反應(yīng)1(Egr-1),而不是c-Jun FOXO1/3a,或B / C-Myb直接transactivates Bim基因表達(dá)調(diào)節(jié)大鼠小腦顆粒神經(jīng)元的凋亡。我們表明,Egr-1是充分必要的神經(jīng)元凋亡。抑制Egr-1活動(dòng)使用dominant-negative突變或擊倒Egr-1使用小型干擾rna導(dǎo)致Bim表達(dá)減少,而超表達(dá)Egr-1導(dǎo)致感應(yīng)的蕩婦。刪除和定點(diǎn)誘變Bim發(fā)起人透露,女子轉(zhuǎn)錄激活主要取決于一個(gè)公認(rèn)的Egr-binding序列核苷酸之間的-56年和-47年開(kāi)始網(wǎng)站的上游。我們還表明,Egr-1綁定到這個(gè)序列響應(yīng)活動(dòng)增加剝奪體外和體內(nèi)。此外,抑制Egr-1綁定Bim發(fā)起人,通過(guò)光神霉素和色霉素A3,減少了活動(dòng)deprivation-induced Bim推廣活動(dòng)的增加和信使核糖核酸和蛋白質(zhì)水平和保護(hù)神經(jīng)元凋亡,進(jìn)一步支持Egr-1-mediated transactivation蕩婦。此外,Bim克服了Egr-1 knockdown-mediated ofapoptosis抑制,而女子擊倒Egr-1誘導(dǎo)細(xì)胞凋亡的增加受損。這些發(fā)現(xiàn)在神經(jīng)元建立Bim Egr-1目標(biāo)基因,揭示小說(shuō)Egr-1 / Bim活動(dòng)不足導(dǎo)致神經(jīng)元凋亡的途徑。 |
3樓2014-03-12 22:40:26
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