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  • Catalog #:2205

  • Scientific Name:N-Hexanoyl-biotin-lactosylceramide

  • Common Name:N-C6:0-Biotin-beta-D-lactosylceramide

  • Empirical Formula:C46H82N4O15S

  • SDS:View Safety Data Sheet

  • Data Sheet:View Data Sheet

  • Formula Weight:963

  • Unit:1 mg

  • Solvent:none

  • Source:semisynthetic

  • Purity:98+%

  • Analytical Methods:TLC, identity confirmed by MS

  • Natural Source:bovine buttermilk

  • Solubility:chloroform/methanol 9:1, DMSO, DMF

  • Physical Appearance:solid

  • Storage:-20℃

  • Dry Ice:No

  • Hazardous:No


Application Notes:

N-己酰-生物素-乳酰基神经酰胺包含生物素单元,通过己酰酸连接物连接到鞘苷部分的胺上,非常适合用于鞘脂研究。 这种生物素结构使乳糖酰胺附着在链霉亲和素、亲和素或任何其他生物素结合蛋白上,使其对底物和毒素的检测非常有用1。 亲和素-生物素复合物是已知蛋白质和配体之间最强的非共价相互作用。 这种键的形成非常迅速,一旦形成,它的pH值、温度、有机溶剂和变性剂都是稳定的。 生物素标签通过减少生物素与乳糖酰神经酰胺的相互作用的6碳连接物附着。 乳酰神经酰胺是许多其他鞘糖脂的前体,同时也作为第二信使和蛋白质受体,使其成为非常重要的有机分子。 许多细胞过程依赖于乳酰神经酰胺,因为它是中性低糖基神经酰胺、硫酸盐和神经节苷脂的底物,所有这些都有自己的重要功能。 乳酰神经酰胺还有助于稳定脂质膜,激活受体分子,并作为某些细菌和毒素的受体。 它作为第二信使的作用已被发现是至关重要的,在其过程中的功能失调可导致癌症和炎症,因为它是中性粒细胞活动和激活抗炎反应的关键 其他具有乳酰神经酰胺第二信使功能的例子有肿瘤坏死因子和血小板源性生长因子。 2 .乳糖神经酰胺的半乳糖水解酶的缺乏导致乳糖神经酰胺病,其特征是乳糖神经酰胺的积累引起原发性神经系统疾病 3 .乳酰神经酰胺在血小板/内皮细胞粘附分子-1的激活中也起重要作用,从而引起单核细胞/淋巴细胞的粘附和衰竭。  

N-Hexanoyl-biotin-lactosylceramide contains a biotin unit attached to the amine of the sphingosine moiety via a hexanoic acid linker and is ideal for use in sphingolipid studies. The biotin structure allows for the attachment of the lactosylceramide to streptavidin, avidin, or any other biotin binding protein making it extremely useful for substrate and toxin detection1. The avidin-biotin complex is the strongest known non-covalent interaction between a protein and ligand. The formation of the bond is very rapid and once formed is stable with regards to pH, temperature, organic solvents, and denaturing agents. The biotin label is attached via a 6-carbon linker reducing the interaction of the biotin with the lactosylceramide. Lactosylceramide is the precursor of many other glycosphingolipids and also functions as a second messenger and protein receptor, making it a very important organic molecule. Many cellular processes are dependent on lactosylceramide since it is the substrate for neutral oligoglycosylceramides, sulfatides and gangliosides, all of which have their own vital functions. Lactosylceramide also helps to stabilize the lipid membrane, activate receptor molecules and acts as a receptor for certain bacteria and toxins. Its role as a second messenger has been found to be vital and dysfunctions in its processes can lead to cancer and inflammation since it is critical to neutrophil activity and in activating anti-inflammatory responses.2 Other examples of lactosylceramide second messenger functions are tumor necrosis factor alpha and platelet-derived growth factor. A deficiency in the enzyme responsible for hydrolyzing the galactose of lactosylceramide leads to lactosylceramidosis, which is characterized by an accumulation of lactosylceramide that causes a primary neurological disorder.3 Lactosylceramide is also important in the activation of platelet/endothelial cell adhesion molecule-1 which causes adhesion and diapedesis of monocytes/lymphocytes.4

1. A. Mukhopadhyay et al. “Direct interaction between the inhibitor 2 and ceramide via sphingolipid-protein binding is involved in the regulation of protein phosphatase 2A activity and signaling” FASEB, Vol. 23(3) pp. 751-763, 2009
2. R. Pannu et al. “A Novel Role of Lactosylceramide in the Regulation of Tumor Necrosis Factor alpha-mediated Proliferation of Rat Primary Astrocytes: IMPLICATIONS FOR ASTROGLIOSIS FOLLOWING NEUROTRAUMA” Journal of Biological Chemistry, Vol. 280 pp. 13742-13751, 2005
3. G. Dawson “Glycosphingolipid levels in an unusual neurovisceral storage disease characterized by lactosylceramide galactosyl hydrolase deficiency: lactosylceramidosis” Journal of Lipid Research, Vol. 13 pp. 207-219, 1972
4. N. Gong “Lactosylceramide recruits PKC and phospholipase A2 to stimulate PECAM-1 expression in human monocytes and adhesion to endothelial cells” Proceedings of the National Academy of Sciences, Vol. 101:17 pp. 6490-6495, 2004