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17-10451

CpGenome Direct Prep Bisulfite Modification Kit (50 Reactions)

The CpGenome Direct Prep Bisulfite Modification Kit allows bisulfite conversion directly from a variety of starting materials, including cultured cells, blood, fresh tissue & fixed tissue samples.

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About This Item

UNSPSC Code:
12161503
eCl@ss:
32161000
NACRES:
NA.84
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Quality Level

manufacturer/tradename

CpGenome

application(s)

genomic analysis

Related Categories

General description

Methylation of cytosines located 5′ to guanosine is known to have a profound effect on the expression of many eukaryotic genes. In normal cells methylation occurs predominantly in CG-poor regions, while CG-rich areas, called CpG-islands remain unmethylated. The exceptions are the extensive methylation of CpG islands associated with transcriptional inactivation of regulatory regions of imprinted genes and genes on the inactive X-chromosome of females. Aberrant methylation of normally unmethylated CpG islands has been documented as a relatively frequent event in immortalized and transformed cells and has been associated with transcriptional inactivation of defined tumor suppressor genes in human cancers. Hundreds of CpG islands are now known to exhibit the characteristic of hypermethylation in tumors resulting in identification of candidate genes that can be interrogated to determine extent of tumor specific transformation.
Unlike other bisulfite modifications approaches that start with isolated genomic DNA, the CpGenome Direct Prep Bisulfite Modification Kit allows simple and reliable bisulfite conversion of DNA directly from a variety of starting materials, including cultured cells, blood, fresh tissue and fixed tissue samples.

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

Research Category
Epigenetics & Nuclear Function

Other Notes

2X Extraction Buffer

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
Replaces: Replaces S7820 (CpGenome Universal DNA Modification Kit).

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 Code

8A - Combustible corrosive hazardous materials

Regulatory Information

新产品
This item has

Certificates of Analysis (COA)

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Li-Min Gao et al.
The American journal of surgical pathology, 40(6), 836-846 (2016-03-15)
Aggressive natural killer cell leukemia (ANKL) is a rare disease with an extremely aggressive clinical course. The etiology of ANKL is unclear with few genetic/epigenetic aberrations described to date. Moreover, misdiagnosis of ANKL is a frequent problem. Clinicopathologic characteristics of
B Leclercq et al.
Environmental pollution (Barking, Essex : 1987), 218, 1074-1088 (2016-09-07)
While the knowledge of the underlying mechanisms by which air pollution-derived particulate matter (PM) exerts its harmful health effects is still incomplete, detailed in vitro studies are highly needed. With the aim of getting closer to the human in vivo conditions and
Effects of 5-aza-2'deoxycytidine on RECK gene expression and tumor invasion in salivary adenoid cystic carcinoma.
Zhou, XQ; Huang, SY; Zhang, DS; Zhang, SZ; Li, WG; Chen, ZW; Wu, HW
Brazilian journal of medical and biological research null
Promoter hypermethylation of the cysteine protease RECK may cause metastasis of osteosarcoma.
Wang, L; Ge, J; Ma, T; Zheng, Y; Lv, S; Li, Y; Liu, S
Tumour Biology : the Journal of the International Society For Oncodevelopmental Biology and Medicine null
Pygopus-2 promotes invasion and metastasis of hepatic carcinoma cell by decreasing E-cadherin expression.
Zhang, S; Li, J; Liu, P; Xu, J; Zhao, W; Xie, C; Yin, Z; Wang, X
Oncotarget null

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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