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Merck
CN

S8001M

CpGenome人甲基化DNA标准品套装

It is intended for use as a positive control in gene methylation studies, such as bisulfite conversion of DNA with the CpGenome Turbo Bisulfite Modification Kit.

别名:

CpGenome甲基化DNA, 人DNA标准品, 甲基化DNA标准品套装

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关于此项目

UNSPSC Code:
12161503
NACRES:
NA.77
eCl@ss:
32161000
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产品名称

CpGenome人甲基化DNA标准品套装, It is intended for use as a positive control in gene methylation studies, such as bisulfite conversion of DNA with the CpGenome Turbo Bisulfite Modification Kit.

biological source

human

form

liquid

species reactivity

human

manufacturer/tradename

CpGenome
Upstate®

solubility

H2O: soluble at 20 °C

application(s)

genomic analysis

shipped in

dry ice

storage temp.

−20°C

Quality Level

相关类别

Application

研究类别
表观遗传学&核功能

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

CpGenome人甲基化DNA标准液从HCT116 DKO细胞中纯化而来——该细胞含有DNA甲基转移酶的基因敲除物DNMT1 (-/-)和DNMT3b (-/-), DNA甲基化率低于5%。该标准已通过 M. SssI 甲基转移酶对所有CpG二核苷酸进行甲基化。它可在基因甲基化研究中作为阳性对照,例如用CpGenome Turbo亚硫酸氢盐修饰试剂盒(货号S7847)对DNA进行亚硫酸氢盐转化。利用CpG WIZ扩增试剂盒,通过甲基化特异性PCR (MSP)技术评估亚硫酸氢盐修饰DNA。

随附材料:

1瓶,含5 µg (20 µL) CpGenome人甲基化DNA标准液,浓度为250 ng/µL。

验证:

用CpGenome Turbo亚硫酸氢盐试剂盒(货号S7847)对CpGenome人甲基化DNA进行甲基化特异性PCR (MSP)。本试验使用了来自CpG WIZ BRCA1扩增试剂盒(货 号S7830)的三组引物:U引物集,重组为未甲基化亚硫酸氢盐修饰DNA;M引物,重组为甲基化亚硫酸氢盐修饰序列;以及W引物,重组为未经亚硫酸氢盐修饰的未甲基化或甲基化DNA。只有M引物形成甲基化的DNA标准品

。CpGenome和CpG WIZ是Serologicals Corporation的商标。 CpG WIZ甲基化产品运用了约翰霍普金斯大学医学院独家许可的技术。 甲基化特异性PCR(MSP)技术包含受美国专利号5,786,146保护。

Physical form

缓冲液液体溶液,含 10 mM Tris-HCl、1 mM EDTA,pH 8.0

Preparation Note

建议储存:自收货之日起,最多可在-20°C下稳定保存6个月。

Legal Information

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

wgk

WGK 1

flash_point_f

does not flash

flash_point_c

does not flash


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相关内容

DNA methylation is an important epigenetic mechanism regulating gene silencing, imprinting, embryonic development, and chromosome stability. DNA methylation occurs on the 5 carbon position of cytosine residues mainly within CpG dinucleotides to form 5-methylcytosines (5-mC). The reaction is catalyzed by DNA methyltransferases (DNMTs). 5-methylcytosines residues may also be hydroxylated by TET enzymes to form 5-hydroxymethylcytosine (5-hmC), which has differing roles from 5-mC. EMD Millipore provides robust tools that enable you to not only detect and quantify 5-mC and 5-hmC, but also to accurately distinguish between these modifications.

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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