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Merck
CN

16-661

Sigma-Aldrich

Magna ChIP® 蛋白A磁珠

Recombinant Protein A covalently bound to magnetic beads for use in chromatin immunoprecipitations (ChIP assays). These protein A beads provide users a more rapid, reproducible & efficient reagent for collecting immunocomplexes vs. agarose beads.

别名:

ChIP magnetic beads, ChIP magnetic A beads, Magnetic Chromatin Immunoprecipitation

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关于此项目

UNSPSC代码:
41105507
eCl@ss:
32160405
NACRES:
NA.52
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质量水平

包装

pkg of 1 mL

制造商/商品名称

Magna ChIP®

储存条件

do not freeze

粒径

~3 μm

运输

wet ice

储存温度

2-8°C

相关类别

一般描述

与磁珠共价结合的重组蛋白A。 这些微珠为用户提供了一种快速,可重现和有效的试剂,可用于收集用于染色质免疫沉淀(ChIP)分析的免疫复合物。 与常规蛋白A琼脂糖珠相比,蛋白A磁珠显著减少了对靶免疫复合物的处理时间和机械应激。

应用

每个ChIP应用使用20 µL微珠混悬液。 包括用于50次沉淀反应的足量试剂。 在通过快速涡旋移液之前,将微珠彻底分散。
用于检测/量化:蛋白A
研究类别
表观遗传学&核功能

外形

液体混悬液。 以含0.01%吐温®-20和0.09%叠氮化钠的磷酸盐缓冲液(pH值7.4)中的磁珠浆液形式提供。

制备说明

自发货之日起在2-8°C下可稳定保存1年。 不得冷冻。

分析说明

使用HeLa核提取物和Magna ChIP® A试剂盒(目录#17-610)通过染色质免疫沉淀(ChIP)进行常规评估。

法律信息

MAGNA CHIP is a registered trademark of Merck KGaA, Darmstadt, Germany
TWEEN is a registered trademark of Croda International PLC

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。

储存分类代码

12 - Non Combustible Liquids

WGK

WGK 2

闪点(°F)

Not applicable

闪点(°C)

Not applicable


分析证书(COA)

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Gerda Lagger et al.
Molecular and cellular biology, 23(8), 2669-2679 (2003-04-01)
The cyclin-dependent kinase inhibitor p21/WAF1/CIP1 is an important regulator of cell cycle progression, senescence, and differentiation. Genotoxic stress leads to activation of the tumor suppressor p53 and subsequently to induction of p21 expression. Here we show that the tumor suppressor
Distinct roles for Sp1 and E2F sites in the growth/cell cycle regulation of the DHFR promoter.
Jensen, D E, et al.
Journal of Cellular Biochemistry, 67, 24-31 (1997)
Malay Choudhury et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(7), 8920-8940 (2020-06-11)
In the current work we show that the profibrotic actions of TGF-β are mediated, at least in part, through a metabolic maladaptation in glutamine metabolism and how the inhibition of glutaminase 1 (GLS1) reverses pulmonary fibrosis. GLS1 was found to

商品

Agarose beads Vs. Magnetic beads in Chromatin Immunoprecipitation (ChIP)

相关内容

Chromatin-immunoprecipitation (ChIP) followed by next generation sequencing (ChIP-seq) of the immunoprecipitated DNA is a powerful tool for the investigation of protein:DNA interactions. To perform ChIP-seq, chromatin is isolated from cells or tissues (with or without chemical crosslinking) and fragmented. Antibodies recognizing chromatinassociated proteins of interest are used to enrich the sample for specific chromatin fragments. The DNA is recovered, sequenced on various NGS platforms, and aligned to a reference genome to determine specific protein binding loci. ChIP-seq studies have increased our knowledge of transcription factor biology, DNA methylation and histone modifications.

"Epigenetics describes heritable changes in gene expression caused by non-genetic mechanisms instead of by alterations in DNA sequence. These changes can be cell- or tissue-specific, and can be passed on to multiple generations. Epigenetic regulation enriches DNAbased information, allowing a cell to vary its response across diverse biological and environmental contexts. Although epigenetic mechanisms are primarily centered in the nucleus, these mechanisms can be induced by environmental signals such as hormones, nutrients, stress, and cellular damage, pointing to the involvement of cytoplasmic and extracellular factors in epigenetic regulation."

Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).

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