MIF 蛋白
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- 抗原 See all MIF 蛋白
- MIF (Macrophage Migration Inhibitory Factor (Glycosylation-Inhibiting Factor) (MIF))
- 蛋白类型
- Recombinant
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宿主
- 人
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资源
- 大肠杆菌(E. Coli)
- 原理
- Recombinant Human MIF Protein
- 序列
- Met 1-Ala115
- 产品特性
- Recombinant Human Macrophage migration inhibitory factor is produced by our E.coli expression system and the target gene encoding Met1-Ala115 is expressed.
- 纯度
- > 95 % as determined by reducing SDS-PAGE.
- 内毒素水平
- < 1.0 EU per μg as determined by the LAL method.
- Top Product
- Discover our top product MIF 蛋白
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- 限制
- 仅限研究用
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- 状态
- Frozen, Liquid
- 缓冲液
- Supplied as a 0.2 μm filtered solution of 20 mM PB,150 mM NaCl,20 % Glycerol, pH 7.4.
- 储存条件
- -20 °C
- 储存方法
- Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
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- 抗原
- MIF (Macrophage Migration Inhibitory Factor (Glycosylation-Inhibiting Factor) (MIF))
- 别名
- MIF (MIF 产品)
- 背景
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Background: Human MIF is a 12.5 kDa, 115 amino acid (aa) nonglycosylated polypeptide that is synthesized without asignal sequence .Secretion occurs nonclassically via an ABCA1 transporter.Pro-inflammatory cytokine.Involved in the innate immune response to bacterial pathogens. The expression of MIF at sites ofinflammation suggests a role as mediator in regulating the function of acrophages in host defense.Counteracts the anti-inflammatory activity of glucocorticoids. Has phenylpyruvate tautomerase anddopachrome tautomerase activity (in vitro), but the physiological substrate is not known. It is not clearwhether the tautomerase activity has any physiological relevance, and whether it is important for cytokineactivity.
Synonym: Macrophage migration inhibitory factor, MIF, MMIF, Glycosylation-inhibiting factor, GLIF, L-dopachrome tautomerase, Phenylpyruvate tautomerase
- 分子量
- 12.5 kDa
- UniProt
- P14174
- 途径
- Regulation of Systemic Arterial Blood Pressure by Hormones, Positive Regulation of Immune Effector Process, Production of Molecular Mediator of Immune Response, Regulation of Carbohydrate Metabolic Process, Feeding Behaviour, Smooth Muscle Cell Migration, Negative Regulation of intrinsic apoptotic Signaling
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