N-Hexanoyl-biotin-sulfatide/N-乙酰基-生物素-硫苷脂

Specifications

• Catalog #:2207

• Scientific Name:N-Hexanoyl-biotin-sulfatide

• Common Name:N-C6:0-Biotin-sulfatide; N-Hexanoyl-biotin-sphingosyl-beta-D-galactoside-3-sulfate

• Empirical Formula:C₄₀H₇₂N₄O₁₃S₂

• SDS:View Safety Data Sheet

• Data Sheet:View Data Sheet

• Formula Weight:881

• Unit:1 mg

• Source:semisynthetic, bovine

• Purity:98+%

• Analytical Methods:TLC; identity confirmed by MS

• Solubility:chloroform/methanol/water, 2:1:0.1; methanol/water 9:1; DMF

• Physical Appearance:solid

• Storage:-20℃

• Dry Ice:No

• Hazardous:No

Description

Application Notes:

N-己酰-生物素-硫酸盐含有一个生物素单元，通过己酰酸连接物附着在鞘氨醇的胺上，非常适合用于鞘脂研究。 这种生物素结构允许硫酸盐附着在链霉亲和素、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磺基半乳糖的相互作用的6-碳连接物附着。 硫化物是一种磺脂，主要在中枢神经系统中发现，是一种髓鞘特异性鞘脂。 白质和灰质中缺乏硫化物与阿尔茨海默病和其他类型的痴呆有关。 载脂蛋白E在硫酸盐的代谢中起着重要的调节作用 2 .脑脊液中产生抗硫化物抗体，导致硫化物缺乏，可能是髓鞘变性的原因，导致多发性硬化症和其他脱髓鞘疾病 异色脑白质营养不良是一种遗传性疾病，其特征是溶酶体芳基硫酸酯酶a缺乏，并随后在神经和内脏组织中积累硫酸酯 硫酸盐还调节少突胶质母细胞的分化。 中枢神经系统(CNS)髓鞘对生长的轴突具有强烈的抑制作用，而存在于中枢神经系统髓鞘中的硫化物已被确定为主要的髓鞘相关轴突生长抑制剂 髓鞘中的硫化物，特别是顺式四碳烯酰硫化物，能刺激cd1受限的自然杀伤T细胞群，这对设计针对中枢神经系统自身免疫性疾病中对髓鞘糖脂反应的T细胞的治疗具有重要意义。  

N-Hexanoyl-biotin-sulfatide contains a biotin unit attached to the amine of the sphingosine via a hexanoic acid linker and is ideal for use in sphingolipid studies. The biotin structure allows for the attachment of the sulfatide 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 sulfo-galactose. Sulfatide is a type of sulfolipid that is found primarily in the central nervous system and is a myelin-specific sphingolipid. A deficiency of sulfatide in white and gray matter has been associated with Alzheimer’s disease and other types of dementia. Apoliprotein E plays an important regulating role in the metabolism of sulfatides.2 The production of anti-sulfatide antibodies in the cerebrospinal fluid, leading to a deficiency in sulfatides, may be a cause of degeneration of the myelin sheath, leading to multiple sclerosis and other demyelinating diseases.3 Metachromatic leukodystrophy is an inherited disorder characterized by a deficiency of the lysosomal enzyme arylsulfatase A and the subsequent accumulation of sulfatide in neural and visceral tissues.4 Sulfatide also regulates the differentiation of oligodendroblasts. Central nervous system (CNS) myelin is strongly inhibitory to growing axons and sulfatides present in the myelin of the CNS have been identified as major myelin-associated axon growth inhibitors.5 Sulfatides in the myelin, especially cis-tetracosenoyl-sulfatides, stimulate a distinct population of CD1d-restricted natural killer T cells giving these sulfatides important implications for the design of therapeutics that target T cells reactive for myelin glycolipids in autoimmune diseases of the central nervous system.6

References:
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. H. Cheng, Y. Zhou, D. M. Holtzman, X. Han “Apolipoprotein E mediates sulfatide depletion in animal models of Alzheimer's disease.” Neurobiology of Aging August 2008
3. Ramesh C. Halder, A. Jahng, I. Maricic and Vipin Kumar “Mini Review: Immune Response to Myelin-Derived Sulfatide and CNS-Demyelination” Neurochemical Research, February, Vol. 32(2): 257, 2007
4. Phillip D. Whitfield, Peter C. Sharp, David W. Johnson, Paul Nelson and Peter J. Meikle “Characterization of Urinary Sulfatides in Metachromatic Leukodystrophy Using Electrospray Ionization-Tandem Mass Spectrometry” Molecular Genetics and Metabolism, May Vol. 73(1): 30, 2001
5. A. Winzeler et al. “The Lipid Sulfatide Is a Novel Myelin-Associated Inhibitor of CNS Axon Outgrowth” The Journal of Neuroscience, vol. 31 pp. 6481- 6492, 2011
6. D. Zajonc et al. “Structural basis for CD1d presentation of a sulfatide derived from myelin and its implications for autoimmunity” The Journal of Experimental Medicine, vol. 202 pp. 1517-1526, 2005