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Merck
CN

16-661

Sigma-Aldrich

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

UNSPSC Code:
41105507
eCl@ss:
32160405
NACRES:
NA.52
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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

Recombinant protein A covalently bound to magnetic beads. These beads provide users a rapid, reproducible and efficient reagent for collecting immunocomplexes for chromatin immunoprecipitations (ChIP) assays. Compared with conventional protein A agarose beads, protein A magnetic beads significantly reduce the handling time and mechanical stress on target immunocomplexes.

Application

Research Category
Epigenetics & Nuclear Function
Use 20 µL of bead suspension per ChIP application. Includes sufficient reagents for 50 precipitation reactions. Disperse beads thoroughly before pipetting by rapid vortex.
Used to detect/quantify: Protein A

Physical form

Liquid suspension. Supplied as magnetic bead slurry in phosphate buffered saline, pH 7.4, containing 0.01% Tween®-20 and 0.09% sodium azide.

Preparation Note

Stable for 1 year at 2-8°C from date of shipment. Do Not Freeze.

Analysis Note

Routinely evaluated by Chromatin immunoprecipitation (ChIP) using HeLa nuclear extracts and the Magna ChIP® A Kit (Cat. #17-610).

Legal Information

MAGNA CHIP is a registered trademark of Merck KGaA, Darmstadt, Germany
TWEEN is a registered trademark of Croda International PLC

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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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Gerda Lagger et al.
Molecular and cellular biology, 23(8), 2669-2679 (2003-04-01)
The cyclin-dependent kinase inhibitor p21/WAF1/CIP1 is an important regulator of cell cycle progression, senescence, and differentiation. Genotoxic stress leads to activation of the tumor suppressor p53 and subsequently to induction of p21 expression. Here we show that the tumor suppressor
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Jensen, D E, et al.
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In the current work we show that the profibrotic actions of TGF-β are mediated, at least in part, through a metabolic maladaptation in glutamine metabolism and how the inhibition of glutaminase 1 (GLS1) reverses pulmonary fibrosis. GLS1 was found to

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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