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Merck

SML2430

Sigma-Aldrich

Kdo2-Lipid A (KLA)

≥90% (HPLC)

别名:

KLA, Kdo2-LipidA, 二[3-脱氧-D-甘露糖基-辛磺酰基]-脂质A (铵盐)

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About This Item

经验公式(希尔记法):
C110H202N2O39P2 · xNH3
分子量:
2238.72 (free acid basis)
分類程式碼代碼:
12352211
NACRES:
NA.77

生物源

Escherichia coli

化驗

≥90% (HPLC)

形狀

solid

儲存溫度

−20°C

SMILES 字串

O=C(O)[C@@]1(O[C@H]2[C@@H](O)C([C@H](O)CO)O[C@](C(O)=O)(OC[C@H]3O[C@@H](OC[C@H]4O[C@H](OP(O)(O)=O)[C@@H](NC(C[C@@H](CCCCCCCCCCC)O)=O)C(OC(C[C@@H](CCCCCCCCCCC)O)=O)[C@H]4O)C(NC(C[C@@H](CCCCCCCCCCC)OC(CCCCCCCCCCC)=O)=O)[C@@H](OC(C[C@@H](CCCCCCCCCCC)OC(CCCCC

相关类别

一般說明

3-脱氧-D-甘露辛酮糖酸(Kdo2-Lipid A)是大多数革兰氏阴性细菌中脂多糖的基本成分,也是维持细菌活力的最小结构成分。它可作为脂多糖的活性成分,通过 Toll 样受体 4 (TLR4) 和髓样分化蛋白 2 (MD2) 的复合物刺激强烈的宿主免疫反应。因此,Kdo2-lipid A 是一种重要的刺激剂,用于研究先天免疫系统机制和开发细菌疫苗佐剂。Kdo2 脂质 A/TLR4 拮抗剂也可用于抗炎干预。Kdo2-lipid A 在 RAW264.7 巨噬细胞中诱导鞘脂的从头生物合成,这对于诱导自噬至关重要。Kdo2-Lipid A 已用于动物动脉粥样硬化模型。

其他說明

溶解性:Kdo2 -Lipid A 可以 1 mg/ml 的浓度溶解在 0.1-0.5% 三乙胺(Sigma 目录编号90335)的溶液中(在沉淀的情况下使用超声处理)。采用超声处理直接溶解在细胞培养基中。存储: Kdo2-lipidA 溶解在 0.1-0.5% 三乙胺(Sigma 目录编号 90335)后 ,分装溶液样并在 -20°C下储存。 该溶液在 -20°C 下可稳定保存 2 个月。

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

No data available

閃點(°C)

No data available


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Kacee Sims et al.
The Journal of biological chemistry, 285(49), 38568-38579 (2010-09-30)
Activation of RAW264.7 cells with a lipopolysaccharide specific for the TLR4 receptor, Kdo(2)-lipid A (KLA), causes a large increase in cellular sphingolipids, from 1.5 to 2.6 × 10(9) molecules per cell in 24 h, based on the sum of subspecies
Philipp Wiesner et al.
Circulation research, 107(1), 56-65 (2010-05-22)
Oxidized low-density lipoprotein (LDL) is an important determinant of inflammation in atherosclerotic lesions. It has also been documented that certain chronic infectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations of atherosclerosis. In addition, low-level but persistent metabolic
Nathanael J Spann et al.
Cell, 151(1), 138-152 (2012-10-02)
Inflammation and macrophage foam cells are characteristic features of atherosclerotic lesions, but the mechanisms linking cholesterol accumulation to inflammation and LXR-dependent response pathways are poorly understood. To investigate this relationship, we utilized lipidomic and transcriptomic methods to evaluate the effect
Christian R H Raetz et al.
Journal of lipid research, 47(5), 1097-1111 (2006-02-16)
The LIPID MAPS Consortium (www.lipidmaps.org) is developing comprehensive procedures for identifying all lipids of the macrophage, following activation by endotoxin. The goal is to quantify temporal and spatial changes in lipids that occur with cellular metabolism and to develop bioinformatic

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