1. 细胞的基础信息

2. 细胞常见的研究有哪些？

a) 研究肾脏的生物学特性

b) 药物筛选及肾脏相关疾病治疗的研发

c) 有关该肾细胞耐药机制的研究

d) 建立细胞模型

3. 细胞相关的文献有哪些？

[1] [1]杨雪晴,孙军峰,李慧昕,等.传染性支气管炎病毒诱导Vero细胞发生自噬促进病毒的复制[J/OL].中国兽医科学,1-9[2024-07-16].

（为探究禽传染性支气管炎病毒（infectious bronchitis virus，IBV）能否诱导细胞自噬及其对病毒复制的影响，

本研究利用IBV细胞适应株CEA接种DF-1和Vero细胞，通过Western-blot、透射电镜和激光共聚焦显微镜检测自噬通路关键蛋白 LC3 和 P62 的表达和分布以及自噬小体的形成情况，并通过自噬抑制剂和诱导剂处理评估了自噬对IBV复制的影响。结果显示，IBV不能在DF-1细胞中诱导LC3的转化，但能够诱导Vero细胞中LC3-II和P62的水平升高，并能在 Vero 细胞中诱导形成自噬小体以及LC3-II向自噬体中的聚集，表明IBV能够诱导Vero细胞发生完整自噬。用自噬抑制剂渥曼青霉素和氯喹处理细胞能够抑制IBV诱导的自噬以及病毒的复制，而用自噬激活剂雷帕霉素处理则能够促进病毒的复制。综上所述，IBV能够在Vero细胞中诱导自噬的发生，从而促进病毒的复制。）

[2] Zhang X, Li P, Zheng Q, Hou J. Lactobacillus acidophilus S-layer protein-mediated inhibition of PEDV-induced apoptosis of Vero cells. Vet Microbiol. 2019;229:159-167.

（To gain insight into the mechanism of Lactobacillus acidophilus (L. acidophilus) S-layer protein antiviral activity, we examined how S-layer protein impacts porcine epidemic diarrhea virus (PEDV) infection and PEDV-induced apoptosis of Vero cells. Pretreatment (exclusion assay), coincubation (competition assay), and post-treatment (displacement assay) of PEDV-infected Vero cells with the S-layer protein was examined. Interestingly, significant inhibition of PEDV by S-layer protein was only observed in the exclusion assay. In Vero cells infected with PEDV, we found that apoptosis was mediated by activation of caspase-8 and caspase-3 in the late stage of infection. When PEDV-infected Vero cells were pretreated with S-layer protein, rates of Vero cell apoptosis were markedly decreased and cell damage was significantly reduced, as evaluated by flow cytometry and microscopy. Detailed analyses showed that the S-layer protein inhibited caspase-8 and caspase-3 activity. Taken together, our results suggest that L. acidophilus S-layer protein plays an inhibitory role during PEDV infection of Vero cells, and that the antagonistic activity of the protein is not via competition with PEDV for binding sites. In addition, the findings suggest that L. acidophilus S-layer protein protects against PEDV-induced apoptosis through reduced caspase-8 and caspase-3 activation in the later stages of infection. This mechanism may represent a novel approach for antagonizing PEDV and other viruses.）