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Merck
CN

L5014

Sigma-Aldrich

脂多糖 来源于大肠杆菌 J5(Rc 突变体)

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别名:
LPS
EC 号:
MDL编号:
UNSPSC代码:
12352201
NACRES:
NA.25

生物来源

Escherichia coli (J5 Rc mutant)

质量水平

形式

lyophilized powder

杂质

<3% Protein (Lowry)

颜色

white to faint beige

溶解性

water: 0.90-1.10 mg/mL, hazy to turbid, colorless to faintly yellow

运输

ambient

储存温度

2-8°C

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生化/生理作用

脂多糖(LPS)位于膜的外层,并且暴露在无包膜菌株的细胞表面。它们有助于维持外层膜的完整性,并保护细胞免受胆汁盐和亲脂性抗生素的破坏。

制备说明

本品溶于水(5 mg/ml)或细胞培养基(1 mg/ml),得到浑浊的淡黄色溶液。以盐水为溶剂时,经过涡旋并加热至70-80 oC后,得到浓度更高但仍然浑浊的溶液(20 mg/ml)。脂多糖分子可在各种溶剂中形成胶束。在水和磷酸盐缓冲盐水中,可观察到混浊的溶液。使用有机溶剂不会得到更澄清的溶液。以甲醇为溶剂将得到含漂浮物的混浊悬浮液,而以水为溶剂将得到均匀的混浊溶液。
通过苯酚-氯仿-石油醚萃取进行制备。

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

警示用语:

Danger

危险声明

危险分类

Acute Tox. 2 Oral

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)


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Xiaoyu Zhang et al.
Oncology letters, 12(2), 1034-1040 (2016-07-23)
Hypoxia-inducible factor-1α (HIF-1α) and toll-like receptor 4 (TLR4) are involved in numerous mechanisms of cancer biology, including cell proliferation and survival; however the interaction of the two factors under hypoxic conditions remains unclear. The present study investigated the in vitro
M Nashleanas et al.
Infection and immunity, 68(3), 1428-1434 (2000-02-26)
The ability to activate macrophages in vitro for nitric oxide production and killing of Leishmania major parasites is dependent on tumor necrosis factor, although L. major-infected mice lacking the TNF receptor p55 (TNFRp55(-/-) mice) or both the TNFRp55 and TNFRp75
Y Wannemuehler et al.
Journal of clinical microbiology, 27(12), 2881-2883 (1989-12-01)
A monoclonal antibody to the lipopolysaccharide of Moraxella bovis is described. In an indirect fluorescent-antibody test, this monoclonal antibody reacted with 39 of 39 strains of M. bovis tested and did not react with 26 nonfermenting gram-negative coccobacilli other than
Sophie E Hussey et al.
Bioscience reports, 33(1), 37-47 (2012-10-12)
Emerging evidence suggests that TLR (Toll-like receptor) 4 and downstream pathways [MAPKs (mitogen-activated protein kinases) and NF-κB (nuclear factor κB)] play an important role in the pathogenesis of insulin resistance. LPS (lipopolysaccharide) and saturated NEFA (non-esterified fatty acids) activate TLR4

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