Quality Level
Application
Disclaimer
General description
Materials Provided:
Two vials, each containing 5 μg (20 μl) of CpGenome Human Non-Methylated DNA Standard or 5 μg (20 μl) of CpGenome Human Methylated DNA Standard, at a concentration of 250 ng/μL.
Validation:
Methylation-specific PCR (MSP) was performed on the DNA after bisulfite modification with the CpGenome Turbo Bisulfite kit (Cat. No. S7847). Three sets of primers from the CpG WIZ BRCA1 amplification kit (Cat. No. S7830) were used in this assay: the U primer set, which anneals to unmethylated bisulfite-modified DNA; M primers, which anneal to methylated bisulfite-modified sequences; and W primers, which anneal to unmethylated or methylated DNA that has not undergone bisulfite modification. Only the M primers generated product for the methylated DNA standard, and only the U primer set amplified the unmethylated Standard.
CpGenome and CpG WIZ are trademarks of Serologicals Corporation. CpG WIZ Methylation Products apply to technologies exclusively licensed from The Johns Hopkins University School of Medicine. Methylation-specific PCR (MSP) technology is covered under U.S. Patent # 5,786,146.
存储类别
10 - Combustible liquids
法规信息
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).
我们的科学家团队拥有各种研究领域经验,包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持