16-661
Magna ChIP® Protein A Magnetic Beads
Recombinant Protein A covalently bound to magnetic beads for use in chromatin immunoprecipitations (ChIP assays). These protein A beads provide users a more rapid, reproducible & efficient reagent for collecting immunocomplexes vs. agarose beads.
Synonym(s):
ChIP magnetic beads, ChIP magnetic A beads, Magnetic Chromatin Immunoprecipitation
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About This Item
Quality Level
packaging
pkg of 1 mL
manufacturer/tradename
Magna ChIP®
storage condition
do not freeze
particle size
~3 μm
shipped in
wet ice
storage temp.
2-8°C
Related Categories
General description
Application
Epigenetics & Nuclear Function
Physical form
Preparation Note
Analysis Note
Legal Information
Disclaimer
Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Articles
Agarose beads Vs. Magnetic beads in Chromatin Immunoprecipitation (ChIP)
Related Content
Chromatin-immunoprecipitation (ChIP) followed by next generation sequencing (ChIP-seq) of the immunoprecipitated DNA is a powerful tool for the investigation of protein:DNA interactions. To perform ChIP-seq, chromatin is isolated from cells or tissues (with or without chemical crosslinking) and fragmented. Antibodies recognizing chromatinassociated proteins of interest are used to enrich the sample for specific chromatin fragments. The DNA is recovered, sequenced on various NGS platforms, and aligned to a reference genome to determine specific protein binding loci. ChIP-seq studies have increased our knowledge of transcription factor biology, DNA methylation and histone modifications.
"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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