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主要文件

MABF96

Sigma-Aldrich

抗-TRACP抗体,克隆9C5

clone 9C5, from mouse

别名:

Tartrate-resistant acid phosphatase type 5, TR-AP, Tartrate-resistant acid ATPase, TrATPase, Type 5 acid phosphatase

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About This Item

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

生物来源

mouse

质量水平

抗体形式

purified antibody

抗体产品类型

primary antibodies

克隆

9C5, monoclonal

种属反应性

human

技术

ELISA: suitable
dot blot: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

同位素/亚型

IgG2bκ

NCBI登记号

UniProt登记号

运输

wet ice

靶向翻译后修饰

unmodified

基因信息

human ... ACP5(54)

一般描述

抗酒石酸酸性磷酸酶5型(TRAcP),也称为Acp5,在骨吸收过程中由破骨细胞分泌。TRAcP的释放受到再吸收细胞因子的刺激,并被降钙素(一种吸收抑制剂)抑制。还已知TRAcP在活性巨噬细胞和树突状细胞中大量表达,并在向T细胞呈递抗原中起重要作用。脂肪组织巨噬细胞释放的非活性TRAcP已显示可引起增生性肥胖,使脂质代谢和胰岛素敏感性保持正常。

免疫原

对应于人TRACP的全长纯化蛋白。

应用

抗TRAcP抗体,克隆9C5检测TRAcP水平,&已发布&验证可用于IH、IP、DB、ELISA、IC & WB。
研究子类别
炎症 & 自身免疫机制
研究类别
炎症 & 免疫学
蛋白质印迹分析: 一个代表性批次已被独立实验室用于WB。(Janckila,A.J.,et al.(1995).Blood.85:2839-2844.)

免疫沉淀分析: 一个代表性批次已被独立实验室用于IP。(Janckila,A.J.,et al.(1995).Blood.85:2839-2844.)

斑点印迹分析: 一个代表性批次已被独立实验室用于DB。(Janckila,A.J.,et al.(1995).Blood.85:2839-2844.)

ELISA分析: 一个代表性批次已被独立实验室用于ELISA。(Janckila,A.J.,et al.(1995).Blood.85:2839-2844.)

免疫细胞化学分析: 一个代表性批次已被独立实验室用于IC。(Janckila,A.J.,et al.(1996).The Journal of Histochemistry and Cytochemistry.44(3):233-244.)

质量

通过免疫组织化学评估毛细胞白血病组织中的大型恶性B细胞。

免疫组织化学分析:该抗体以1:500稀释度在毛细胞白血病组织的大型恶性B细胞中检测到TRAcP。

目标描述

计算分子量36 kDa

外形

形式:纯化
纯化的小鼠单克隆IgG2bκ,溶于含0.1 M Tris-甘氨酸(pH 7.4)、150 mM NaCl和0.05%叠氮化钠的缓冲液中。
蛋白G

储存及稳定性

自接收之日起,在2-8°C下可稳定保存1年。

分析说明

对照
毛细胞白血病组织中的大恶性B细胞

其他说明

浓度:关于批次特定浓度请参见检验报告。

免责声明

除非我们的目录或产品随附的其他公司文件中另有说明,否则我们的产品预期仅用于研究用途,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对人类或动物的任何类型的消费或应用。

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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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Christina Møller Andreasen et al.
Bone, 173, 116787-116787 (2023-05-08)
Although failure to establish a vascular network has been associated with many skeletal disorders, little is known about what drives development of vasculature in the intracortical bone compartments. Here, we show that intracortical bone resorption events are coordinated with development
Nicolai Ernlund Lassen et al.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 32(7), 1395-1405 (2017-02-09)
It is well known that bone remodeling starts with a resorption event and ends with bone formation. However, what happens in between and how resorption and formation are coupled remains mostly unknown. Remodeling is achieved by so-called basic multicellular units
Xenia G Borggaard et al.
Frontiers in molecular biosciences, 9, 896841-896841 (2022-07-02)
The strictly regulated bone remodeling process ensures that osteoblastic bone formation is coupled to osteoclastic bone resorption. This coupling is regulated by a panel of coupling factors, including clastokines promoting the recruitment, expansion, and differentiation of osteoprogenitor cells within the
Julia Brun et al.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 35(12), 2458-2469 (2020-08-11)
The physiological functions of platelet-derived growth factor receptors (PDGFRs) α and β in osteoblast biology and bone metabolism remain to be established. Here, we show that PDGFRA and PDGFRB genes are expressed by osteoblast-lineage canopy and reversal cells in close
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Clinical & experimental metastasis, 34(3-4), 261-271 (2017-04-28)
Prostate cancer (PCa) patients with bone metastases are primarily treated with androgen deprivation therapy (ADT). Less pronounced ADT effects are seen in metastases than in primary tumors. To test if acute effects of ADT was enhanced by concurrent inhibition of

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