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Merck
CN

AB5605

抗4-羟基壬烯醛抗体

serum, Chemicon®

别名:

4-HNE

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关于此项目

UNSPSC代码:
12352203
eCl@ss:
32160702
NACRES:
NA.41
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生物来源

goat

质量水平

抗体形式

serum

抗体产品类型

primary antibodies

克隆

polyclonal

种属反应性

human

制造商/商品名称

Chemicon®

技术

ELISA: suitable
western blot: suitable

运输

dry ice

靶向翻译后修饰

unmodified

一般描述

自由基对膜脂质的过氧化作用是在正常细胞更新和正常衰老过程中发生的一个受控良好的持续过程。 由于暴露于卤代烃,过量的酒精滥用和急性或慢性铁超负荷,还存在与肝损伤相关的自由基生成和脂质过氧化增加的不受控制的过程。 过度自由基生成和脂质过氧化是动脉粥样硬化、糖尿病、遗传性血色素沉着病、癌症和神经退行性疾病(如阿尔茨海默′病和帕金森′病)等疾病的病因。4-羟基壬烯醛(HNE)是一种在w-6-不饱和脂肪酸氧化过程中释放的高反应性、细胞毒性醛。 除了磷脂和核酸外,HNE能与蛋白质的巯基或组氨酸和赖氨酸基团有效反应,形成稳定的HNE-蛋白质加合物。 通过这种对生物分子的HNE修饰,认为HNE发挥了其细胞毒性效应。 这种多功能分子可能被认为是“第二毒性信使”,它可以传播和增强初始自由基事件。 据信这是氧化应激期间观察到的细胞病理学效应的主要原因。 在许多疾病状态下都检测到了高水平4-HNE,表明该醛在其发病机理中有一定参与。 4-HNE的一些突出的病理生化作用是其刺激纤维发生和炎症。 这表明对几种慢性疾病的发病机理的潜在贡献,其进展由炎症反应支持并以纤维化为特征。 4-HNE能通过干扰细胞周期蛋白和蛋白激酶的活性并抑制凋亡反应来调节细胞增殖,因此在致癌中也可能起作用。

免疫原

4-HNE。

应用

抗4-羟基壬烯酸抗体可检测4-羟基壬烯酸水平&已发表 & 验证可用于 ELISA & WB。
研究子类别
氧化应激
研究类别
神经科学
蛋白质印迹: 对人类阿尔茨海默′病脑裂解物为1:3000。
ELISA:>1:10,000

最佳工作稀释度必须由最终用户进行确定。

生化/生理作用

对4-羟基壬烯醛(4-HNE)具有特异性。
该AB5605抗体识别的HNE部分是独立于物种的生化修饰。 因此,抗4-HNE抗体应具有广泛的物种反应性。

外形

山羊抗血清。 含0.1%叠氮化钠的液体

制备说明

自收到之日起,在-20° C以未稀释的等分试样可保存 6 个月。 应避免反复冻/融循环。 请勿储存于自除霜冰箱中。

法律信息

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

免责声明

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

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储存分类代码

12 - Non Combustible Liquids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Effects of ?-3 PUFAs supplementation on myocardial function and oxidative stress markers in typical Rett syndrome.
Maffei, S; De Felice, C; Cannarile, P; Leoncini, S; Signorini, C; Pecorelli, A; Montomoli et al.
Mediators of Inflammation null
Neuronal PPARgamma deficiency increases susceptibility to brain damage after cerebral ischemia.
Zhao, X; Strong, R; Zhang, J; Sun, G; Tsien, JZ; Cui, Z; Grotta, JC; Aronowski, J
The Journal of Neuroscience null
Lourdes Lorigados Pedre et al.
Behavioral sciences (Basel, Switzerland), 8(6) (2018-06-13)
Oxidative stress (OS) has been implicated as a pathophysiological mechanism of drug-resistant epilepsy, but little is known about the relationship between OS markers and clinical parameters, such as the number of drugs, age onset of seizure and frequency of seizures
Claudio De Felice et al.
Neurobiology of disease, 68, 66-77 (2014-04-29)
Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers
Redox imbalance and morphological changes in skin fibroblasts in typical Rett syndrome.
Signorini, C; Leoncini, S; De Felice, C; Pecorelli, A; Meloni, I; Ariani, F; Mari et al.
Oxidative Medicine and Cellular Longevity null

相关内容

"Redox reactions are powerful chemical processes that involve the reduction and oxidation of proteins and metabolites found in living things. The mechanisms that regulate them are key to maintaining homeostasis and the balance between good health and disease pathology. Oxidative stress is the state where the delicate balance of redox biology is upset, and the pathology of oxidative stress are the cellular consequences to such an imbalance."

"Aging: getting older, exhibiting the signs of age, the decline in the physical (and mental) well-being over time, leading to death. Since the beginning of time, man has been obsessed with trying to slow down, stop, or even reverse the signs of aging. Many have gone as far as experimenting with nutritional regimens, eccentric exercises, fantastic rituals, and naturally occurring or synthetic wonder-elements to evade the signs of normal aging. Biologically speaking, what is aging? And what does the latest research tell us about the possibility of discovering the elusive “fountain of youth”? Many advances in our understanding of aging have come from systematic scientific research, and perhaps it holds the key to immortality. Scientifically, aging can be defined as a systems-wide decline in organismal function that occurs over time. This decline occurs as a result of numerous events in the organism, and these events can be classified into nine “hallmarks” of aging, as proposed by López-Otin et al. (2013). Several of the pathologies associated with aging are a direct result of these events going to extremes and may also involve aberrant activation of proliferation signals or hyperactivity. The hallmarks of aging have been defined based on their fulfillment of specific aging related criteria, such as manifestation during normal aging, acceleration of aging if experimentally induced or aggravated, and retardation of aging if prevented or blocked, resulting in increased lifespan. The nine hallmarks of aging are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. The biological processes underlying aging are complex. By understanding the hallmarks in greater detail, we can get closer to developing intervention strategies that can make the aging process less of a decline, and more of a recline."

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