EZ-Magna ChIP^® HiSens染色质免疫沉淀试剂盒

Superior enrichment, low background. With performance proven for both qPCR and ChIP-seq analysis, the Magna ChIP™ HiSens kit may be the only ChIP kit you’ll ever need. Outperforming any competing kit, this revolutionary approach to ChIP enables enrichment from both low and high amounts of input chromatin while also delivering low backgrounds and high signal-to-noise ratios for ultra-sensitive detection.

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.

Chromatin immunoprecipitation (ChIP) has been widely adapted for the study of gene-specific and genome-wide distribution of specific DNA- and RNA-binding proteins or protein modifications. Similar to standard protein immunoprecipitation assays, ChIP involves isolation of immunocomplexes using a solid medium, such as agarose or magnetic beads, coupled to either IgG binding recombinant protein A or protein G. In a typical ChIP experiment either protein A or G is selected for enrichment depending on the antibody isotype. However, proteins A and G possess differing affinities for human and mouse IgGs. Complicating this choice, for some antibody isotypes there is affinity for both protein A and G. In addition, we have observed that independent of the isotype the affinity of a specific antibody for protein A or G can vary depending on the specific clone, purification method, and source.

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).