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Merck
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主要文件

L2137

Sigma-Aldrich

脂多糖 来源于肠沙门氏菌 明尼苏达血清型

purified by gel-filtration chromatography

别名:

LPS

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About This Item

MDL號碼:
分類程式碼代碼:
12352201
NACRES:
NA.25

生物源

Salmonella enterica (Serotype minnesota)

品質等級

形狀

lyophilized powder

純化經由

gel-filtration chromatography

雜質

<1% Protein

顏色

white

溶解度

water: 4.90-5.10 mg/mL, cloudy to hazy, colorless

運輸包裝

ambient

儲存溫度

2-8°C

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一般說明

脂多糖(LPS)是革兰氏阴性菌细胞壁的特征性成分。LPS及其脂质A部分可通过Toll样受体4(TLR4)刺激先天免疫系统细胞,TLR4是Toll样受体蛋白家族的成员,它能识别常见的病原体相关分子模式(PAMP)。
This product is extracted from Salmonella Minnesota and purified by gel filtration. The source strain is ATCC 9700. Mechanisms of complement activation by LPS of both rough and smooth strains of Salmonella Minnesota were studied by immunoassay of the activation products.

應用


  • TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling: This study explores the signaling pathways activated by lipopolysaccharides from Salmonella enterica serotype Minnesota, demonstrating that TRPV4 is not involved, advancing understanding of immune responses to bacterial endotoxins (Wang et al., 2023).

生化/生理作用

Lipopolysaccharides (LPS) are localized in the outer layer of the membrane and are, in noncapsulated strains, exposed on the cell surface. They contribute to the integrity of the outer membrane, and protect the cell against the action of bile salts and lipophilic antibiotics.

準備報告

The product is soluble in water (5 mg/ml) or cell culture medium (1 mg/ml) yielding a hazy, faint yellow solution. A more concentrated, though still hazy, solution (20 mg/ml) has been achieved in aqueous saline after vortexing and warming to 70-80 oC. Lipopolysaccharides are molecules that form micelles in every solvent. Hazy solutions are observed in water and phosphate buffered saline. Organic solvents do not give clearer solutions. Methanol yields a turbid suspension with floaters, while water yields a homogeneously hazy solution.

其他說明

To gain a comprehensive understanding of our extensive range of Lipopolysaccharides for your research, we encourage you to visit our Carbohydrates Category page.

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Melanie R Shakespear et al.
The Journal of biological chemistry, 288(35), 25362-25374 (2013-07-16)
Broad-spectrum inhibitors of histone deacetylases (HDACs) constrain Toll-like receptor (TLR)-inducible production of key proinflammatory mediators. Here we investigated HDAC-dependent inflammatory responses in mouse macrophages. Of the classical Hdacs, Hdac7 was expressed at elevated levels in inflammatory macrophages (thioglycollate-elicited peritoneal macrophages)
Pei Ching Low et al.
The Journal of cell biology, 190(6), 1053-1065 (2010-09-15)
Phosphoinositide 3-kinase (PI3K) p110 isoforms are membrane lipid kinases classically involved in signal transduction. Lipopolysaccharide (LPS)-activated macrophages constitutively and abundantly secrete proinflammatory cytokines including tumor necrosis factor-α (TNF). Loss of function of the p110δ isoform of PI3K using inhibitors, RNA-mediated
Victor Meseguer et al.
Nature communications, 5, 3125-3125 (2014-01-22)
Gram-negative bacterial infections are accompanied by inflammation and somatic or visceral pain. These symptoms are generally attributed to sensitization of nociceptors by inflammatory mediators released by immune cells. Nociceptor sensitization during inflammation occurs through activation of the Toll-like receptor 4
Kaustav Das Gupta et al.
Cell reports, 30(8), 2712-2728 (2020-02-27)
Histone deacetylases (HDACs) drive innate immune cell-mediated inflammation. Here we identify class IIa HDACs as key molecular links between Toll-like receptor (TLR)-inducible aerobic glycolysis and macrophage inflammatory responses. A proteomic screen identified the glycolytic enzyme pyruvate kinase M isoform 2
Anna Lünemann et al.
Journal of immunology (Baltimore, Md. : 1950), 181(9), 6170-6177 (2008-10-23)
Microglia are resident macrophage-like APCs of the CNS. To avoid escalation of inflammatory processes and bystander damage within the CNS, microglia-driven inflammatory responses need to be tightly regulated and both spatially and temporally restricted. Following traumatic, infectious, and autoimmune-mediated brain

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