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- 详细信息
- 文献和实验
- 技术资料
- 英文名:
Immortalized Human Umbilical Vein Fibroblasts
- 库存:
100万
- 供应商:
欣润生物
- 肿瘤类型:
否
- 细胞类型:
永生化
- ATCC Number:
无
- 品系:
人源
- 组织来源:
脐静脉
- 相关疾病:
无
- 物种来源:
人源
- 免疫类型:
不详
- 细胞形态:
成纤维细胞样
- 是否是肿瘤细胞:
否
- 器官来源:
脐静脉
- 运输方式:
常温
- 年限:
/
- 生长状态:
悬浮生长
- 规格:
T25方瓶
永生化人脐静脉成纤维细胞简介:
产品描述:除毛细血管和毛细淋巴管以外,血管壁从管腔面向外一般依次分为内膜、中膜和外膜,血管壁内还有营养血管和神经分布。外膜由疏松结缔组织组成,其中含螺旋状或纵向分布的弹性纤维和胶原纤维。血管壁的结缔组织细胞以成纤维细胞为主,当血管受损伤时,成纤维细胞具有修复外膜的能力。
产品货号:IH1014
产品类型: 原代细胞建立的永生化
传代能力: 30代左右
产品形态: 成纤维细胞样
培养基:永生化人脐静脉成纤维细胞专用完全培养基,产品编号:IH1014-5
支原体:呈阴性
产品培养条件:37℃,5%CO2
发货方式:常温T25方瓶运输
货期:1周左右货期
永生化人脐静脉成纤维细胞白光图
Curcumin inhibits cell cycle progression of immortalized human umbilical vein endothelial (ECV304) cells by up-regulating cyclin-dependent kinase inhibitor, p21WAF1/CIP1, p27KIP1 and p53.
To elucidate possible mechanisms of anti-angiogenic activity by curcumin, we performed cDNA microarray and found that curcumin modulated cell cycle related gene expression. For further confirmation, DNA contents and expression levels of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CDKIs) were examined by FACS analysis and Western blotting, respectively. Curcumin was found to induce G0/G1 and/or G2/M phase cell cycle arrest, up-regulate CDKIs, p21WAF1/CIP1, p27KIP1, and p53, and slightly down-regulate cyclin B1 and cdc2 in ECV304 cells. However, expression level of other cyclins and CDKs were not changed by curcumin. We, therefore, conclude that the up-regulation of CDKIs by curcumin plays a critical role in the regulation of cell cycle distribution in these cells, which may have a major role in anti-angiogenic activity of curcumin.
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文献和实验Chicken intestinal epithelial cells were obtained from NEWGAINBIO company. Cells were cultured on 37℃, with 5% CO2, in the Ham’s F-12 Nutrient (DMEM/12) that contained the following supplementations: fetal bovine serum (5%), in-sulin (5 µg/mL), transferrin (5 µg/mL), selenium (5 ng/mL), epidermal growth factor (5 ng/mL) and penicillin-streptomycin (100–100 U/mL) for cell culturing (full DMEM/12). Experiments were performed with chicken intestinal epithelial cells and working solutions were prepared with plain DMEM/12 without supplementation. For the investigations, cells were seeded onto 96-well, 24-well or 6-well polystyrene cell culture plates.
Primary hVICs (passage 2) were cultured to 50–60% confluence and infected with pGMLV-SV40T-puro lentivirus (NewgainBio, Wuxi, China) at a multiplicity of infection of 80 supplemented with 5 µg/mL polybrene (Sigma-Aldrich, Buchs, Switzerland).
Tissue was cultured until cells became visible around the tissue, and when the fusion reached 90% (FIGURE 1A) §ask ¦lled with the prepared culturing medium was sent to the company for further immortalisation. Cell immortalisation was done for cell stability and longer-term use. Immortalised cells were cultured with 10% FBS and 1% PS in the DMEM medium. After the cells multiplied and merged, they were routinely passed and grown ( NEWGAINBIO Inc. Wuxi, Jiangsu, China) (FIGURE 1B-C).
Mouse primary cultured renal vascular ECs and VSMCs were obtained from Newgainbio company, which were tested by Factor VIII and α-smooth muscle actin (α-SMA), the marker of ECs and VSMCs. RNeasy Mini Kit was used for RNA extraction, and the above protocols were repeated.
Porcine primary colon epithelial cells (Newgainbio company, Wuxi,China) were cultured in Dulbecco's Modified Eagle's Medium (Solarbio, Beijing, China) containing 10 % fetal bovine serum (BioInd, Kiryat shmona, Lsrael) at 37 ◦C and 5 % CO2 humidity.
基因编辑再次升级!领域大牛刘如谦 Cell 发文开发新工具,可安全高效进行体内基因编辑
4 BE-eVLPs 支持有效、高效的基因编辑,并且显示出最小的脱靶编辑效率和 DNA 整合风险。 图片来源:Cell v4 BE-eVLPs 有效地编辑人类原代细胞和小鼠细胞 为了进一步探索 v4 BE-eVLPs 的效用,他们评估了其在体外靶向和编辑多种原代人类或小鼠细胞的能力。在转导含有纯合子 COL7A1(R185X)突变的原代人类成纤维细胞中,他们观察到高于 95% 的修复效率。这种高效率在小鼠模型的原代成纤维细胞中也得到了重现。 这些结果验证了 v4 BE-eVLPs 的活性并不局限于细胞系
三句话读懂一篇 CNS:肥胖导致脱发;逆转慢性心脏病;杂交土豆问世...
basis of substrate recognition and translocation by human ABCA4。 该研究解析了 ABCA4 三种不同状态的原子分辨率冷冻电镜结构,揭示了 ABCA4 对脂质底物的转运机制。 图 3:来源 Nature Communications 4. Nature:转录开关调控心脏病逆转 成纤维细胞活化使得慢性心脏病进一步恶化。 2021 年 6 月 23 日,美国格莱斯顿研究所 Deepak Srivastava 教授团队在 Nature 发表研究
/? p1} T9q3w;Wp9j 大多数肿瘤细胞有遗传学改变,如失去二倍体核型、呈异倍体或多倍体等。肿瘤细胞群常由多个细胞群组成,有干细胞系和数个亚系,并不断进行着适应性演变。 (七)其它 肿瘤细胞在体外不易生长的原因可能由于:① 依赖性:肿瘤细胞虽有较强克隆生长力,但仍有一定的群体性或与其它细胞相依存关系。一是肿瘤细胞与肿瘤细胞的相互依存,二是肿瘤细胞与基质成纤维细胞的依赖。体外分散培养和排除成纤维细胞后也会同时消除或减弱这些依存
技术资料







