S8003
Standardy ludzkiego DNA CpGenome 5-mC i 5-hmC
The CpGenome 5-mC & 5-hmC Human DNA Standards provides two samples of human genomic DNA from the same individual.
Wybierz wielkość
| Gabaryty przesyłki | SKU | Dostępność | Cena netto |
|---|---|---|---|
| 1 set | Przewidywany termin wysyłki24 kwietnia 2026zKuehne + Nagel Sp. z o.o. | 3070,00 zł |
Informacje o tej pozycji
3070,00 zł
Przewidywany termin wysyłki24 kwietnia 2026Szczegóły
General description
Application
Epigenetics & Nuclear Function
Physical form
Preparation Note
Other Notes
One vial of human spleen DNA, 5µg
Legal Information
Disclaimer
1 of 1
Ta pozycja | |||
|---|---|---|---|
| Quality Level 100 | Quality Level 100 | Quality Level 100 | Quality Level 100 |
| species reactivity human | species reactivity - | species reactivity mouse | species reactivity human |
| shipped in dry ice | shipped in - | shipped in - | shipped in dry ice |
| manufacturer/tradename CpGenome | manufacturer/tradename - | manufacturer/tradename CpGenome, Upstate® | manufacturer/tradename CpGenome, Upstate® |
Klasa składowania
10 - Combustible liquids
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Powiązane treści
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).
Numer pozycji handlu globalnego
| SKU | NUMER GTIN |
|---|---|
| S8003 | 04053252823756 |