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General description
Key Features
- Bisulfite conversion directly from cells, tissues, blood and FFPE samples without DNA purification
- Sensitive bisulfite-conversion from as few as 10 cells or as low as 50 pg of input DNA
- Fast and simple, streamlined protocol for one-step bisulfite conversion
- In-column desulfonation allows recovery of DNA without additional precipitation steps for more consistent results
- Suitable for downstream analysis by methlylation specific PCR, restriction digestion, sequencing, microarray hybridization, etc.
Application
Epigenetics & Nuclear Function
Other Notes
Modification Reagent
Conversion Buffer
Resuspension Buffer
Equilibration Buffer
Binding Buffer
Wash Buffer I
Wash Buffer II
Elution Buffer
Proteinase K
Proteinase K Storage Buffer
Desalting Columns
Collection Tubes
Disclaimer
Storage Class Code
8A - Combustible corrosive hazardous materials
Regulatory Information
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.
Unlike other bisulfite modification approaches that start with isolated genomic DNA, the CpGenome™ Direct Prep, and CpGenome™ Direct Prep-96 kits allow simple and efficient bisulfite conversion of DNA directly from your sample. Avoid the need to isolate genomic DNA and perform bisulfite modification of unmethylated cytosines starting with fresh or frozen tissues, cultured cells, whole blood, buffy coat, biopsies, or FFPE (formalin-fixed paraffin-embedded) samples.
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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