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Merck
CN

SAB4200071

Sigma-Aldrich

大鼠单克隆抗-FLAG® 抗体

clone 6F7, purified from hybridoma cell culture

别名:

抗 ddddk, 抗 dykddddk

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About This Item

MDL编号:
UNSPSC代码:
12352203
NACRES:
NA.32

生物来源

rat

偶联物

unconjugated

抗体形式

purified from hybridoma cell culture
purified immunoglobulin

抗体产品类型

primary antibodies

克隆

6F7, monoclonal

形式

buffered aqueous solution

种属反应性

all

技术

immunoprecipitation (IP): 2.5-5.0 μg using lysates of transiently transfected cells expressing C-terminal-FLAG-tagged protein
western blot: 0.5-1.0 μg/mL using extracts of transiently transfected cells expressing C-terminal-FLAG-tagged protein

同位素/亚型

IgG1

免疫原序列

(DYKDDDDK)

运输

dry ice

储存温度

−20°C

一般描述

FLAG单克隆抗体®(大鼠IgG1同种型)来源于小鼠骨髓瘤细胞和用FLAG®肽免疫大鼠的脾细胞融合而产生的杂交瘤6F7。从生物反应器中生长的杂交瘤细胞的培养上清中纯化抗体。

FLAG单抗®识别N-端、
C端和内部FLAG标签融合蛋白。特别推荐该产品用于识别C-端FLAG®标签融合蛋白。
表位标签提供的方法可定位各种类型细胞中的基因产物、研究蛋白和蛋白复合物的拓扑结构、识别相关蛋白,并在没有蛋白特异性抗体时对新鉴定、丰度低或免疫原性低的蛋白进行表征。FLAG® 肽序列标签可以在N-端、前面有甲硫氨酸残基的N-端、C-端或在靶蛋白的内部位置进行。FLAG也可以与其他标签一起使用。短FLAG® 标签或序列及其高亲水性倾向于降低蛋白表达干扰、蛋白水解成熟、抗原性和功能。

N-端FLAG® 肽序列含有独特的肠激酶切割位点,使其可以从纯化的融合蛋白中完全去除。Cu2+ 离子催化的从融合蛋白切去C-端FLAG® 肽也有报道。在大鼠和小鼠Mg2+依赖性蛋白b-磷酸酶以及人类和牛类的酶中发现了一种基序,其八个氨基酸残基中有五个与FLAG肽相同。

免疫原

FLAG肽

DYKDDDDK

应用

大鼠抗FLAG®单克隆抗体已用于:
  • 染色质免疫沉淀(ChIP)
  • 蛋白印迹
  • 免疫共沉淀
  • 流式细胞分析

更多产品信息,请访问我们的FLAG®应用页面。
在我们的 FLAG® 文献 门户网站可浏览其他应用的参考文献。

外形

0.01M 磷酸缓冲盐溶液,pH 7.4,含 15mM 叠氮化钠。

法律信息

ANTI-FLAG is a registered trademark of Merck KGaA, Darmstadt, Germany
FLAG is a registered trademark of Merck KGaA, Darmstadt, Germany

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闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

常规特殊物品

分析证书(COA)

输入产品批号来搜索 分析证书(COA) 。批号可以在产品标签上"批“ (Lot或Batch)字后找到。

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访问文档库

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Laboratory Investigation; a Journal of Technical Methods and Pathology, 99(6), 736-736 (2019)
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Li Q, et al
Journal of Experimental & Clinical Cancer Research, 36(1), 85-85 (2017)
Rahul Bhowmick et al.
Journal of virology, 87(12), 6840-6850 (2013-04-12)
p53, a member of the innate immune system, is triggered under stress to induce cell growth arrest and apoptosis. Thus, p53 is an important target for viruses, as efficient infection depends on modulation of the host apoptotic machinery. This study

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