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Merck
CN
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主要文件

657012

Sigma-Aldrich

兔抗酪氨酸羟化酶多克隆抗体

liquid, Calbiochem®

别名:

Anti-Tyrosine Hydroxylase Antibody

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About This Item

UNSPSC代码:
12352203
NACRES:
NA.41

生物来源

rabbit

质量水平

抗体形式

purified antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

liquid

不包含

preservative

种属反应性(根据同源性预测)

all

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
avoid repeated freeze/thaw cycles

同位素/亚型

IgG

运输

wet ice

储存温度

−70°C

靶向翻译后修饰

unmodified

一般描述

亲和纯化的兔多克隆抗体。识别约60 kDa的酪氨酸羟化酶蛋白。
在识别冈田酸处理的PC12细胞中约60 kDa的酪氨酸羟化酶蛋白。
该抗酪氨酸羟化酶兔pAb经验证可用于斑点印迹、免疫印迹、免疫荧光、冷冻切片检测酪氨酸羟化酶

免疫原

大鼠
纯化SDS变性大鼠嗜铬细胞瘤酪氨酸羟化酶

应用

斑点杂交(1:1000)

免疫印迹(1:1000)

免疫荧光(1:1000)

冰冻切片(1:1000;见应用参考)

警告

毒性:标准处理(A)

外形

在150 mM NaCl、10 mM HEPES、50%丙三醇、0.01% BSA、pH 7.5中。

重悬

初次解冻后,分装冻存(-70°C)。

法律信息

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

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储存分类代码

10 - Combustible liquids

WGK

WGK 1


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The in vivo firing patterns of ventral midbrain dopamine neurons are controlled by afferent and intrinsic activity to generate sensory cue and prediction error signals that are essential for reward-based learning. Given the absence of in vivo intracellular recordings during
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Given the recent in vitro discovery that the free soluble oligosaccharide of GM1 is the bioactive portion of GM1 for neurotrophic functions, we investigated its therapeutic potential in the B4galnt1+/- mice, a model of sporadic Parkinson's disease. We found that
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Neuronal Ca2+ sensor proteins (NCS) transduce changes in Ca2+ homeostasis into altered signaling and neuronal function. NCS-1 activity has emerged as important for neuronal viability and pathophysiology. The progressive degeneration of dopaminergic (DA) neurons, particularly within the Substantia nigra (SN)
A K M Ghulam Muhammad et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 15(19), 6113-6127 (2009-10-01)
Glioblastoma multiforme is a deadly primary brain cancer. Because the tumor kills due to recurrences, we tested the hypothesis that a new treatment would lead to immunological memory in a rat model of recurrent glioblastoma multiforme. We developed a combined
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eLife, 7 (2018-11-14)
Extinction of fear responses is critical for adaptive behavior and deficits in this form of safety learning are hallmark of anxiety disorders. However, the neuronal mechanisms that initiate extinction learning are largely unknown. Here we show, using single-unit electrophysiology and

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