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L4516

Sigma-Aldrich

脂多糖 来源于大肠杆菌 0127:B8

BioXtra, suitable for cell culture, γ-irradiated

别名:

LPS

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About This Item

CAS号:
93572-42-0
EC 号:
297-473-0
MDL编号:
MFCD00212998
UNSPSC代码:
12352211
NACRES:
NA.75

生物来源

Escherichia coli (O127:B8)

质量水平

200

无菌性

γ-irradiated

产品线

BioXtra

表单

lyophilized powder

纯化方式

gel-filtration chromatography

技术

cell culture | mammalian: suitable

杂质

<1% Protein (Lowry)

溶解性

H2O: 5 mg/mL, slightly hazy

储存温度

2-8°C

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应用

来自Escherichia coli 0127:B8脂多糖用于：
  • 研究LPS诱导小鼠巨噬细胞存活
  • 诱导牛PBMC分泌细胞因子
  • 研究LPS诱导促炎环境高易感巨噬细胞细胞凋亡。
  • 进行BV2和BV2-LC3细胞自吞噬实验。
  • 激活人单核细胞，巨噬细胞和小鼠小胶质细胞
  • 诱导293T细胞穿透素-3
脂多糖（LPS）是革兰氏阴性菌细胞壁的特征组分。LPS及其脂质A部分可通过能够识别常见的病原体相关分子模式（PAMP）的Toll样受体蛋白家族成员Toll样受体4（TLR4）刺激先天性免疫系统细胞。

生化/生理作用

脂多糖（LPS）是革兰氏阴性菌细胞壁的特征组分。LPS和它的脂质A单体通过Toll样受体4（TLR4）激活天然免疫系统细胞。作为免疫原抗原，它增强了对于可溶性抗原的免疫反应。

重悬

脂多糖以经γ-射线处理的冻干粉形式提供。如需重悬，可将1 ml无菌的平衡盐溶液或组织培养基加入至小瓶（1 mg）中并轻轻晃动直至粉末溶解。重悬后的产品可采用无菌的平衡盐溶液或组织培养基进一步被稀释至所需的工作浓度。

其他说明

为了全面了解我们针对客户研究提供的各种脂多糖产品，建议您访问我们的碳水化合物分类页面。

象形图

Skull and crossbones
GHS06

警示用语：

Danger

危险声明

H300

危险分类

Acute Tox. 2 Oral

储存分类代码

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number
0000370464
0000370464
0000242816
0000185322
019M4180V

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Journal of neuroinflammation, 14(1), 198-198 (2017-10-05)
Several G-protein-coupled receptors (GPCRs) have been shown to be important signaling mediators between neurons and glia. In our previous screening for identification of nerve injury-associated GPCRs, G-protein-coupled receptor 84 (GPR84) mRNA showed the highest up-regulation by microglia after nerve injury.
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Cells, 9(9) (2020-09-23)
Bone marrow-derived mast cells (BMMCs) are often used as a model system for studies of the role of MCs in health and disease. These cells are relatively easy to obtain from total bone marrow cells by culturing under the influence
Hua Liu et al.
International journal of clinical and experimental pathology, 6(4), 660-668 (2013-04-11)
The aim of the present study was to explore the role of receptor tyrosine kinases (RTKs) in the regulation of expression of PTX-3, a protector in atherosclerosis. Human monocytic U937 cells were infected with a shRNA lentiviral vector library targeting
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