17-611
Magna ChIP® G - Chromatin Immunoprecipitation Kit
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Description
22 individual chromatin immunoprecipitation (ChIP) reactions using magnetic G beads.
Niveau de qualité
Conditionnement
kit of 22 assay(s)
Technique(s)
immunoprecipitation (IP): suitable
Description générale
Caractéristiques et avantages
- Faster: Magnetic protein G beads allow for the entire ChIP protocol to be done in as little as a day! All reagents to process your samples are included - you don′t have to spend valuable time making them.
- Easier: Spin columns make DNA purification easier and more reliable - no more messy phenol-chloroform extractions.
Conditionnement
Notes préparatoires
Autres remarques
- Magnetic Protein G Beads
- ChIP Dilution Buffer
- Low Salt Wash Buffer
- High Salt Wash Buffer
- LiCl Wash Buffer
- TE Buffer
- Cell Lysis Buffer
- Nuclear Lysis Buffer
- ChIP Elution Buffer (w/o Proteinase K)
- 10X Glycine
- 10X PBS
- Protease Inhibitor Cocktail II
- Proteinase K
- Spin Filters
- Collection Tubes
- Bind Reagent A
- Wash Reagent B
- Elution Reagent C
Informations légales
Clause de non-responsabilité
Mention d'avertissement
Danger
Mentions de danger
Conseils de prudence
Classification des risques
Acute Tox. 4 Oral - Aquatic Chronic 3 - Eye Irrit. 2 - Flam. Liq. 2 - Skin Irrit. 2
Code de la classe de stockage
3 - Flammable liquids
Point d'éclair (°F)
55.4 °F
Point d'éclair (°C)
13 °C
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Contenu apparenté
"Epigenetics describes heritable changes in gene expression caused by non-genetic mechanisms instead of by alterations in DNA sequence. These changes can be cell- or tissue-specific, and can be passed on to multiple generations. Epigenetic regulation enriches DNAbased information, allowing a cell to vary its response across diverse biological and environmental contexts. Although epigenetic mechanisms are primarily centered in the nucleus, these mechanisms can be induced by environmental signals such as hormones, nutrients, stress, and cellular damage, pointing to the involvement of cytoplasmic and extracellular factors in epigenetic regulation."
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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