Dna Methylation Proteins


 Creative BioMart Dna Methylation Proteins Product List
 Dna Methylation Proteins Background

Among the genome-wide data now available, DNA methylation has attracted a lot of attention. Catalyzed by DNA methyltransferase (DNMT) enzymes, a methyl group is attached to the carbon 5 position of cytosines located adjacent to guanines. It is one of the most well studied mechanisms of epigenetic gene regulation, that is, heritable changes in gene expression that are caused by factors other than changes of the DNA sequence. CpG stands for “-C-phosphate-G-” which is a cytosine and a guanine separated by one phosphate in linear sequence. It is used to distinguish from the CG base-pair of cytosine and guanine. CpG islands are DNA regions with a high frequency of CpG sites. CpGs residing in CpG islands have a different methylation status compared with CpGs residing in other regions. Usually, the methylated CpG sites are followed by spontaneous deamination which converts 5-methylcytosine to thymine. That is why methylation is rare in CpG islands. It is well known that methylation of DNA may silence gene expression: the methylated DNA may impede the binding of DNA transcription factors and/or lead to binding of methyl-CpG-binding domain proteins that lead to changes in chromatin structure. However, with further comprehension of DNA methylation, researchers found methylation also plays a role in many other biological processes, including embryonic development, X-chromosome inactivation, genomic imprinting, and preservation of chromosome stability. Many factors can affect DNA methylation, such as age, gene mutation, cell culture, and microenvironment. In addition, smoking has been shown to alter DNA methylation.

DNA methylation has been related to many kinds of diseases, especially cancer. It has been proposed that carcinogenesis is associated with DNA with increased methylation, named hypermethylation, in some sequences. For example, aberrant hypermethylation may inactivate tumor suppressor genes. However, it is worth noting that DNA with decreased methylation, named hypomethylation, may also correlate with cancer development. Current research focuses on building genome-wide DNA methylation profiles. For example, special genomic signatures have been developed to describe and characterize cancers. In terms of copy number alterations, GBM has characteristic chromosome 7 amplification and chromosome 10 deletion while breast invasive carcinoma has characteristic chromosome 2 and chromosome 8 amplification.

On the other hand, most human DNA methylation marks are likely stable, making them useful as disease biomarkers. Analyzing data from cancer patients, we observe a widespread disruption of the human DNA methylation profile. The human DNA methylation profile plays a role in the etiology of numerous other complex diseases including asthma, coronary heart disease, and bipolar disorder.

Recent advances in biomedical technology make it possible to perform large-scale measurements of DNA methylation across the human genome. As a result, the methylated state of each CpG site and its location in the human genome can be identified. Thus, some of the methods used to detect disease susceptibility loci for genetic variants can be applied to detect disease susceptibility CpG sites. As a primary manufacturer of recombinant proteins, Creative Biomart provides protein product of several sources, grades and formulations for DNA methylation research applications.

 

DNA methylation reference

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2. Phillips T. The role of methylation in gene expression[J]. Nature Education, 2008, 1(1): 116.

Horvath S. DNA methylation age of human tissues and cell types[J]. Genome biology, 2013, 14(10): 1-20.

3. Paz M F, Fraga M F, Avila S, et al. A systematic profile of DNA methylation in human cancer cell lines[J]. Cancer research, 2003, 63(5): 1114-1121.

4. Guida F, Sandanger T M, Castagné R, et al. Dynamics of smoking-induced genome-wide methylation changes with time since smoking cessation[J]. Human molecular genetics, 2015, 24(8): 2349-2359.

5. Ehrlich M. DNA hypomethylation in cancer cells[J]. Epigenomics, 2009, 1(2): 239-259.

6. Ehrlich M. DNA methylation in cancer: too much, but also too little[J]. Oncogene, 2002, 21(35): 5400-5413.

7. Foley D L, Craig J M, Morley R, et al. Prospects for epigenetic epidemiology[J]. American journal of epidemiology, 2009, 169(4): 389-400.

8. Laird P W. Principles and challenges of genome-wide DNA methylation analysis[J]. Nature Reviews Genetics, 2010, 11(3): 191-203.

9. Hackenberg M, Barturen G, Carpena P, et al. Prediction of CpG-island function: CpG clustering vs. sliding-window methods[J]. BMC genomics, 2010, 11(1): 327.