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Merck
CN

17-229

Acetyl-Histone H4 Immunoprecipitation (ChIP) Assay Kit

Acetyl-Histone H4 Immunoprecipitation (ChIP) Assay Kit used to immunoprecipitate transcriptionally active chromatin from mammalian cells using anti-Acetyl-Histone H4, ChIP grade rabbit antiserum.

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UNSPSC Code:
12161503
NACRES:
NA.52
eCl@ss:
32161000
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manufacturer/tradename

Upstate®

technique(s)

immunoprecipitation (IP): suitable

NCBI accession no.

UniProt accession no.

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dry ice

Quality Level

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General description

For use to immunoprecipitate transcriptionally active chromatin from mammalian cells using anti-Acetyl-Histone H4, ChIP grade rabbit antiserum. Detection of the gene or promoter of interest in immunoprecipitated chromatin must be empirically determined by the researcher using quantitative PCR or Southern slot-blot analysis, using promotor specific primers or probe.

Application

Acetyl-Histone H4 Immunoprecipitation (ChIP) Assay Kit used to immunoprecipitate transcriptionally active chromatin from mammalian cells using anti-Acetyl-Histone H4, ChIP grade rabbit antiserum.

Packaging

Kit capacity: 22 assays

Other Notes

Anti-acetyl-Histone H4 (Cat.# 06-866)

Protein A agarose/Salmon Sperm DNA (Cat.# 16-157)

All necessary buffers

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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.

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Aquatic Chronic 3 - Eye Irrit. 2

存储类别

10 - Combustible liquids

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Guocheng He et al.
Molecular and cellular biology, 22(9), 2965-2973 (2002-04-10)
Repression of human immunodeficiency virus type 1 (HIV-1) transcription may contribute to the establishment or maintenance of proviral quiescence in infected CD4(+) cells. The host factors YY1 and LSF cooperatively recruit histone deacetylase 1 (HDAC1) to the HIV-1 long terminal
Priya Kapoor-Vazirani et al.
Cancer research, 68(16), 6810-6821 (2008-08-15)
Epigenetic silencing of tumor suppressor genes in human cancers is associated with aberrant methylation of promoter region CpG islands and local alterations in histone modifications. However, the mechanisms that drive these events remain unclear. Here, we establish an important role
Lata Balakrishnan et al.
Journal of molecular biology, 365(1), 18-30 (2006-10-24)
SV40 chromosomes undergoing transcription operationally defined by the presence of RNA polymerase II (RNAPII) were immune-selected with antibody to RNAPII and subjected to secondary chromatin immunoprecipitation with antibodies to hyperacetylated or unacetylated H4 or H3. Immune selection fragmentation and immunoprecipitation
Shaojing Chang et al.
Journal of immunology (Baltimore, Md. : 1950), 181(12), 8372-8381 (2008-12-04)
Forming and removing epigenetic histone marks at gene loci are central processes in differentiation. Here, we explored mechanisms establishing long-range H4 acetylation marks at the Ifng locus during Th1 lineage commitment. In Th0 cells, histone deacetylase (HDAC)-Sin3A complexes recruited to
V Perissi et al.
Genes & development, 13(24), 3198-3208 (2000-01-05)
Retinoic acid and thyroid hormone receptors can act alternatively as ligand-independent repressors or ligand-dependent activators, based on an exchange of N-CoR or SMRT-containing corepressor complexes for coactivator complexes in response to ligands. We provide evidence that the molecular basis of

相关内容

"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."

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