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Merck
CN

S8001U

CpGenome人非甲基化DNA标准品套装

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

别名:

Human Non-Methylated DNA Standard

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关于此项目

UNSPSC Code:
12161503
NACRES:
NA.31
eCl@ss:
32161000
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产品名称

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

form

liquid

species reactivity

human

manufacturer/tradename

CpGenome
Upstate®

solubility

H2O: soluble

application(s)

genomic analysis

shipped in

dry ice

Quality Level

相关类别

General description

CpGenome人未甲基化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%。它可在基因甲基化研究中作为阴性对照,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人非甲基化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人非甲基化DNA进行甲基化特异性PCR (MSP)。CpG WIZ BRCA1扩增试剂盒(货号S7830)的三组引物用于本试验: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U引物产生本标准品

。CpGenome和CpG WIZ是Serologicals Corporation的商标。 CpG WIZ甲基化产品应用技术,该技术已获得约翰霍普金斯大学医学院的独家许可。 甲基化特异性PCR(MSP)技术包含在美国专利#5,786,146中。

Legal Information

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

存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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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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