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S8003

CpGenome 5-mC & 5-hmC Human DNA Standards

The CpGenome 5-mC & 5-hmC Human DNA Standards provides two samples of human genomic DNA from the same individual.

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About This Item

UNSPSC Code:
12161503
NACRES:
NA.31
eCl@ss:
32161000
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Product Name

CpGenome 5-mC & 5-hmC Human DNA Standards, The CpGenome 5-mC & 5-hmC Human DNA Standards provides two samples of human genomic DNA from the same individual.

species reactivity

human

manufacturer/tradename

CpGenome
Upstate®

shipped in

dry ice

Quality Level

Related Categories

Physical form

Aqueous bufer containing 10 mM Tris-HCl;0.1mM EDTA; pH 8.0.

Preparation Note

Stable for 12 months at -20°C from date of receipt.

Legal Information

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

General description

The CpGenome 5-mC & 5-hmC Human DNA Standards provides two samples of human genomic DNA from the same individual. This genomic DNA contains physiological levels of 5-mC and 5-hmC,that have been precisely quantified by LC/MS analysis. These matched human standards are useful as positive controls in DNA methylation assays designed to detect or quantify 5-mC (5-methylcytosine) and/or 5-hmC (5-hydroxymethylcytosine) modifications.

Other Notes

One vial of human brain DNA, 5µg

One vial of human spleen DNA, 5µg

Application

Research Category
Epigenetics & Nuclear Function
The CpGenome 5-mC & 5-hmC Human DNA Standards provides two samples of human genomic DNA from the same individual.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Storage Class

10 - Combustible liquids

Regulatory Information

高风险级别生物产品-Merck
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Certificates of Analysis (COA)

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Related Content

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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