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Merck
CN

AB5613P

抗脑源性神经营养因子抗体

Chemicon®, from rabbit

别名:

Prepro-Abrineurin, Pro-Abrineurin, Prepro-BDNF, Pro-BDNF, Prepro-Brain-derived neurotrophic factor, Pro-Brain-derived neurotrophic factor

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Technique(s):
western blot: suitable
immunohistochemistry: suitable
Conjugate:
unconjugated
Application:
western blot
immunohistochemistry
Clone:
polyclonal
Citations:
10
Species reactivity:
mouse, rat, human
Uniprot accession no.:
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产品名称

抗脑源性神经营养因子抗体, Chemicon®, from rabbit

technique(s)

western blot: suitable
immunohistochemistry: suitable

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

mouse, rat, human

manufacturer/tradename

Chemicon®

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... BDNF(627)

Application

抗脑源性神经营养因子抗体,pro是用于免疫组化和蛋白质印迹的抗体proBDNF。
研究子类别
神经化学&神经营养因子

神经炎症&疼痛
研究类别
神经科学
蛋白质印迹:1:2,000

免疫组化:1:2,000

最佳工作稀释度必须由最终用户进行确定。

Biochem/physiol Actions

该多克隆抗体可检测前体BDNF和前BDNF,以及前体BDNF/前BDNF衍生的含有前肽序列的N末端片段(a.a.19-128),但不检测含前肽序列的成熟BDNF或C末端片段。与其他神经营养因子原无交叉反应。

Disclaimer

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。

General description

脑源性神经营养性因子(UniProt P23560;也称为Abrineurin,BDNF,Neurotrophin)由人的BDNF(也称为BULN2)基因(基因ID 627)编码。BDNF是神经营养因子(也称为神经营养因子)NGF家族的成员,是中枢和外周神经系统中特定神经元亚群的分化和存活所必需的。神经营养因子家族由至少四种蛋白质组成,包括NGF,BDNF,NT3和NT4/5。BDNF通过高亲和细胞表面受体gp145/trkB发出信号来介导其神经营养特性。BDNF最开始是由一个信号肽(a.a.1-18)和前肽(aa19-128)序列产生的,去除该序列会产生成熟的BDNF(a.a.129-247)。
观察值约35 kDa(糖基化前体/前BDNF),约50-65 kDa(糖基化前体/前BDNF二聚体)和约26-28 kDa(非糖基化前体/前BDNF或糖基化前体/前BDNF N末端片段)。由于糖基化和/或二聚化,目标条带似乎大于计算的分子量27.82/28.87/29.82/37.12/31.12 kDa(人前体-BDNF亚型1/2/3/4/5)和25.77/26.82/27.77/35.07/29.06 kDa(人前-BDNF亚型1/2/3/4/5)。某些裂解液可能会出现未表征的条带。

Immunogen

对应于人BDNF前肽序列内区域的KLH偶联的线性肽。
表位:前肽。

Physical form

从10 mM PBS中进行冻干。用20 μL无菌蒸馏水复溶。

Preparation Note

在接收之日起,将冻干物料在-20°C下保存长达6个月。复溶后以未稀释状态在-20°C下保存长达 6个月。应避免反复冻/融循环。可添加(1:1)甘油(ACS级或更优级)以获得额外的稳定性。

Legal Information

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

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存储类别

13 - Non Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Kevin K Caldwell et al.
Pharmacology, biochemistry, and behavior, 90(4), 614-624 (2008-06-19)
Prenatal ethanol exposure is associated with an increased incidence of depressive disorders in patient populations. However, the mechanisms that link prenatal ethanol exposure and depression are unknown. Several recent studies have implicated reduced brain-derived neurotrophic factor (BDNF) levels in the
April P Neal et al.
Toxicological sciences : an official journal of the Society of Toxicology, 116(1), 249-263 (2010-04-09)
Lead (Pb(2+)) exposure is known to affect presynaptic neurotransmitter release in both in vivo and cell culture models. However, the precise mechanism by which Pb(2+) impairs neurotransmitter release remains unknown. In the current study, we show that Pb(2+) exposure during
Oscar V Torres et al.
The international journal of neuropsychopharmacology, 21(3), 281-290 (2017-11-23)
The continuing epidemic of methamphetamine addiction has prompted research aimed at understanding striatal dysfunctions potentially associated with long-term methamphetamine use. Here, we investigated transcriptional and translational alterations in the expression of neurotrophic factors in the rat striatum at 30 days
Marion Rodier et al.
PloS one, 9(3), e92416-e92416 (2014-03-29)
Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular
Mauro Ceccanti et al.
Addiction biology, 21(4), 776-787 (2015-05-06)
Ethanol (EtOH) exposure during pregnancy induces cognitive and physiological deficits in the offspring. However, the role of paternal alcohol exposure (PAE) on offspring EtOH sensitivity and neurotrophins has not received much attention. The present study examined whether PAE may disrupt

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