1. 細胞的基礎信息

2. 細胞常見的研究有哪些？

a) 研究腎臟的生物學特性

b) 藥物篩選及腎臟相關疾病治療的研發

c) 有關該腎細胞耐藥機制的研究

d) 建立細胞模型

3. 細胞相關的文獻有哪些？

[1] [1]楊雪晴,孫軍峰,李慧昕,等.傳染性支氣管炎病毒誘導Vero細胞發生自噬促進病毒的復制[J/OL].中國獸醫科學,1-9[2024-07-16].

（為探究禽傳染性支氣管炎病毒（infectious bronchitis virus，IBV）能否誘導細胞自噬及其對病毒復制的影響，

本研究利用IBV細胞適應株CEA接種DF-1和Vero細胞，通過Western-blot、透射電鏡和激光共聚焦顯微鏡檢測自噬通路關鍵蛋白 LC3 和 P62 的表達和分布以及自噬小體的形成情況，并通過自噬抑制劑和誘導劑處理評估了自噬對IBV復制的影響。結果顯示，IBV不能在DF-1細胞中誘導LC3的轉化，但能夠誘導Vero細胞中LC3-II和P62的水平升高，并能在 Vero 細胞中誘導形成自噬小體以及LC3-II向自噬體中的聚集，表明IBV能夠誘導Vero細胞發生完整自噬。用自噬抑制劑渥曼青霉素和氯喹處理細胞能夠抑制IBV誘導的自噬以及病毒的復制，而用自噬激活劑雷帕霉素處理則能夠促進病毒的復制。綜上所述，IBV能夠在Vero細胞中誘導自噬的發生，從而促進病毒的復制。）

[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.）