内质网应激

已有的研究证实内质网应激与细胞凋亡发生密切相关，内质网应激途径是细胞凋亡途径之一。

The existing researches have demonstrated that endoplasmic reticulum stress is relevant to apoptosis and the endoplasmic reticulum stress path is one of the apoptotic paths .

肝癌细胞N-乙酰氨基葡萄糖基转移酶V表达受阻与内质网应激之间的关系

Relationship between blocking of N-acetylglucosaminyltransferase V in hepatocarcinoma cells and cellular endoplasmic reticulum stress

p53基因在内质网应激诱导的晶状体上皮细胞凋亡中的作用

The Effect of p53 on Endoplasmic Reticulum Stress-induced Apoptosis of Lens Epithelial Cells

衣霉素诱导的内质网应激可能在衣霉素对TRAIL的这种致敏性中发挥作用。

Tunicamycin-induced ER stress seems to play an important role in tunicamycin-mediated up-regulation of TRAIL receptors .

而细胞内的DCN在外界因素作用下，可能通过内质网应激（ERstress），经泛素-蛋白酶体系统调节降解。

However , intracellular DCN under external factors , can be degraded by Ubiquitin proteasome pathway through ER stress .

Caspase-12短发夹状RNA在内质网应激性凋亡中的作用

Mechanism of apoptosis induced by ER stress through siRNA against caspase-12

过表达肌浆网钙ATP酶2a抑制缺氧诱导心肌细胞内质网应激及凋亡的研究

Inhibition of Endoplasmic Reticulum Stress and Apoptosis in Cultured Hypoxic Cardiomyocytes by Sarcoplasmic Reticulum Calcium ATPase 2a Overexpression

其中，Bcl-2家族蛋白尤为重要，因为内质网应激诱导的细胞凋亡可以被过表达的Bcl-2或其同源性抗凋亡分子所抑制。

Among them , Bcl-2 family proteins appear critical , as ER stress-induced apoptosis can be inhibited by over-expression of Bcl-2 or its anti-apoptotic homologs .

肝脏IR损伤发生机制尚不明确，可能与细胞凋亡、活性氧、线粒体损伤和内质网应激等方面有关。

The mechanism of hepatic IR injury is elusive , which could be associated with apoptosis , reactive oxygen species , mitochondrial permeability transition and endoplasmic reticulum stress .

多种病理条件，如缺血、缺氧或中毒等刺激下，诱导细胞发生以伴侣蛋白表达及非折叠蛋白反应启动为特征的内质网应激（ERstress）。

Many pathological stimulation , such as ischemia , hypoxia and poison , induces ER stress , which is characterized as overexpression of ER molecular chaperone and unfolded protein response ( UPR ) .

我们的结果显示JNK激活持续的时间是决定内质网应激下细胞存活的重要因素。

We show that the duration of JNK activation is critical for cell survival upon ER stress .

TNF-α是否可以通过内质网应激导致B16细胞自噬有待进一步研究。

But whether endoplasmic reticulum stress could trigger autophagy induced by TNF - α need to be elucidated .

抑制MEK对内质网应激诱导乳腺癌细胞凋亡的增敏作用

Inhibition of MEK sensitizes human breast carcinoma cells to endoplasmic reticulum pathway 's apoptosis

文章对脑缺血再灌注诱导内质网应激和UPR的研究进展做了综述。

This article reviews the recent progress in ER stress and UPR induced by cerebral ischemic-reperfusion .

最近研究表明除了caspase依赖的细胞凋亡途径外，还存在内质网应激诱导的细胞凋亡途径。

Recent studies have shown that in addition to caspase dependent apoptotic pathway , there also exists the endoplasmic reticulum stress-induced apoptotic pathway .

从本论文的第一部结果我们得出结论：ATRA通过加剧GnT-V-AS/7721细胞中的内质网应激诱导细胞凋亡。

In the first part of this work , we report that ATRA induces apoptosis in GnT-V-AS / 7721 cells via ER stress .

硫氧还蛋白具有保护多巴胺能神经元免受MPTP所致内质网应激损伤，然而这一作用的分子机理还不十分清楚。

Trx protects neuron from ER stress-mediated cytotoxicity induced by MPTP , and the molecular mechanism is still unclear .

JNK信号途径通过内质网应激反应介导心肌梗死后心力衰竭小鼠心肌组织的凋亡

C-Jun N-terminal protein kinase signaling pathway mediates cardiac myocyte apoptosis in mouse congestive heart failure after myocardial infraction via endoplasmic reticulum stress

UPR联合SREBP-1c在内质网应激致大鼠NASH形成中的作用及意义

The Role and Significance of UPR Combined with SREBP-1c Mediated by Endoplasmic Reticulum Stress in the Development of NASH in Rats

二.内质网应激和泛素-蛋白酶体系统可能是PD多巴胺能神经元凋亡的关键因素，内质网应激的早期调节过程就存有泛素-蛋白酶体系统对异常蛋白的降解活动。

Endoplasmic reticulum stress and the ubiquitin-proteasome system may be the PD dopaminergic neuronal apoptosis key factors . Endoplasmic reticulum stress adjustment in the early has contained activity of the ubiquitin-proteasome system degradation to abnormal proteins .

在细胞水平，硫氧还蛋白诱导物GGA可以缓解MPP+引起的内质网应激，从而抑制细胞凋亡。

GGA , an inducer of Trx , inhibited the ER stress induced by MPP + in vitro .

以上的所有结果表明，ATRA通过加剧GnT-V-AS/7721细胞中的内质网应激诱导细胞凋亡。这为我们提供了一个ATRA诱导肝癌细胞发生凋亡的新机制。

These results suggest that ATRA intensifies the ER stress triggered in GnT-V-AS / 7721 cells , which represents a novel mechanism of ATRA to induce apoptosis .

作为对内质网应激的响应，细胞形成了一条称为未折叠蛋白反应（UPR）的自我保护信号转导通路。

In response to ER stress , cells have developed a self-protective signal transduction pathway termed the unfolded protein response ( UPR ) .

胃腺癌细胞在内质网应激下Mcl-1表达水平的升高能够阻碍其诱导的细胞凋亡。

Gastric adenocarcinoma cells that express increased levels of Mcl-1 under ER stress are more resistant to ER stress-induced apoptosis .

此外，研究还表明内质网应激反应的标志性蛋白是GRP78/Bip.在疾病的早期，GRP78/Bip表达上调是对细胞的保护性反应，也是ERS的应激标志。

In addition , the study also showed that the endoplasmic reticulum stress response iconic protein is GRP78 / Bip upward in early the disease expression .

目的探讨caspase-12表达变化与内质网应激介导小鼠原代肝细胞凋亡的关系。

Objective To investigate the relationship between caspase-12 activation and ER stress mediated apoptosis of primary mouse hepatocytes .

为了检测GCs诱导小鼠腹腔巨噬细胞内质网应激的作用，以及明确ERS在低浓度GCs诱导免疫刺激中的作用。

In order to test the hypothesis that GCs induces ERS in mice peritoneal macrophages , and to elucidate the role of ERS in low concentrations of GCs-induced immunostimulation .

结论：1.脾阴虚糖尿病脑病大鼠学习记忆障碍可能与内质网应激PERK信号途径被启动有关。

The impaired learning and memory ability of spleen-yin deficiency diabetic encephalopathy may relate to the initiating of the PERK signaling pathway of ERS . 2 .

结论Ec可诱导人白血病HL60细胞内质网应激反应性细胞凋亡，凋亡的发生与蛋白质合成抑制、Caspase12的活化有关。

Conclusion Ec can induce endoplasmic reticulum stress-related apoptosis in HL-60 cells . The underlying mechanisms are protein synthesis inhibition through eIF2 α phosphorylation and Caspase 12 activation .

然而，如果脑缺血诱导的内质网应激严重且持续时间长，UPR最终会启动细胞凋亡通路，导致神经元死亡。

However , if ER stress induced by cerebral ischemia is severe and prolonged , UPR ultimately initiates an apoptotic pathway , resulting in neuronal death .