• Unfolded proteins accumulate during ER stress and ER resident proteins GRP78 and GRP94 protect cells against ER dysfunction.

    内质受压时未折叠蛋白积累,内质网驻留蛋白GRP78GRP94保护细胞免于内质功能异常。

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  • Objective To investigate the expression of the glucose regulated protein (GRP78, GRP94) in rats during focal cerebral ischemia.

    目的研究灶性脑缺血时调控蛋白(GRP78GRP94)表达

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  • Elevated protein expression of GRP78 was correlated positively with the content of MDA and HCY in plasma and the index of liver fibrosis (P<0.01).

    表达增高GRP78蛋白分别血浆MDAHCY水平以及纤维化指数显著正相关(P<0.01)。

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  • Whether propofol in clinical dose affects the levels of GRP78 in normal liver cell is not clear, and further research is needed to resolve this question.

    临床剂量异丙酚正常细胞GRP78水平是否影响清楚有待进一步研究。

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  • Results: After LLLI preconditioning, increased VEGF and GRP78 expression, as well as the enhanced SOD activity and inhibited MDA production, was observed.

    结果LLLI预处理显著提高了梗死后心肌组织中vegfGRP78表达及SOD活性,降低了MDA的含量。

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  • Methods: icariin induced cultured rabbit vascular smooth muscle cell apoptosis, in situ hybridization in rabbit plaque GRP78 gene expression levels of the organization.

    方法淫羊藿甙诱导培养血管平滑肌细胞凋亡组织原位杂交观察凋亡基因GRP78斑块组织中的表达水平

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  • Normal cells respond to ER stress by increasing transcription of genes encoding ER-resident molecular chaperones such as GRP94, GRP78 and PDI to facilitate protein folding.

    细胞这种应激反应增加一系列内质分子伴侣GRP94GRP78PDI等的表达。

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  • Objective To evaluate the expression level of glucose regulating protein 78(GRP78) in the model of Parkinson's disease(PD)induced by 6-Hydroxydopamine(6-OHDA) in PC12 cells.

    目的探讨神经毒素6-羟基多巴胺(6-OHDA诱导PC12细胞帕金森PD模型GRP78表达

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  • AIM: to explore the effect of glucose-regulated protein 78 (GRP78) expression on the biological behaviors of hepatocellular carcinoma cells with different metastatic potentials.

    目的研究葡萄糖调节蛋白78 (GRP78)不同转移潜能肝癌细胞株内表达及其肝癌细胞生物学行为影响

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  • Objective: To observe the nature of glucose-regulated protein 78 (GRP78) in atherosclerotic tissue and the possible mechanisms of icariin atherosclerosis prevention and treatment.

    目的观察葡萄糖调节蛋白基因78 (GRP78)动脉粥样硬化组织中的表达,探讨淫羊藿甙防治动脉粥样硬化可能机制

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  • AIM: To investigate the effect of high glucose on the expression of an endoplasmic reticulum stress marker glucose-regulated protein 78 (GRP78), and explore its underlying mechanism.

    目的观察慢性处理血管内皮细胞内质应激标志蛋白葡萄糖调节蛋白78 (GRP78)表达影响及其作用机制

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  • Conclusion: PC has a protective effect on cerebral IR injury, which may related to increased GRP78 and decreased CHOP expression, and to inhibition of the ERS-induced apoptosis pathway.

    结论PC脑缺血再灌注损伤大鼠具有保护作用机制可能与其增加GRP78表达、拮抗chop表达、阻断内质网应激(ERS)启动凋亡通路有关

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  • Conclusion Endoplasmic reticulum-self regulated system was started through the increased expressions of GRP78 and GRP94 after striatum ischemia in rats, so as to attenuated cerebral ischemic injury.

    结论大鼠纹状体缺血可能通过GRP78GRP94表达升高启动内质网自稳调节系统

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  • Conclusion Endoplasmic reticulum-self regulated system was started through the increased expressions of GRP78 and GRP94 after striatum ischemia in rats, so as to attenuated cerebral ischemic injury.

    结论大鼠纹状体缺血可能通过GRP78GRP94表达升高启动内质网自稳调节系统

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