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Merck
CN

17-409

EZ-Magna ChIP® G - 染色质免疫沉淀试剂盒

Single day chromatin immunoprecipitation (ChIP) kit containing all necessary reagents to perform 22 individual chromatin immunoprecipitation (ChIP) reactions using magnetic G beads. Control primers included.

别名:

Magnetic ChIP Kit, Magnetic Chromatin Immunoprecipitation

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关于此项目

UNSPSC代码:
12161503
eCl@ss:
32161000
NACRES:
NA.52
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质量水平

制造商/商品名称

Magna ChIP®

技术

immunoprecipitation (IP): suitable

运输

dry ice

相关类别

一般描述

染色质免疫沉淀(ChIP)是一种强大的技术,可用于绘制与染色体DNA相关的蛋白质的体内分布图。这些蛋白质可以是组蛋白亚基和翻译后修饰或其他染色质相关蛋白质,例如转录因子,染色质调节剂等。此外,ChIP可以用于鉴定与这些蛋白质相关的基因组区域,或者相反地,用于鉴定与基因组的特定区域相关的蛋白质。ChIP方法通常涉及蛋白质-DNA和蛋白质-蛋白质交联,交联染色质的片段化以及随后用对靶蛋白特异的抗体对染色质进行免疫沉淀。与靶蛋白复合分离的DNA片段可以通过多种方法鉴定,包括PCR,DNA微阵列和DNA测序。可以进行标准或定量PCR以验证特定的DNA序列(基因组的基因或区域)是否与靶蛋白相关。ChIP与启动子或基因组平铺微阵列(ChIP芯片)的组合可通过精确的分辨率在全基因组范围内鉴定染色质相关蛋白的DNA结合位点。或者,由免疫沉淀的染色体DNA(ChIP-Seq)构建的文库的高通量测序是ChIP芯片的有力替代方法,可在哺乳动物基因组中绘制蛋白质-DNA各种相互作用。
染色质免疫沉淀(ChIP)是一种重要的技术,使研究人员能够分析蛋白质与基因组DNA的体内各种相互作用。 只要存在针对蛋白的良好抗体,就可以使用该技术分析任何与染色质相关或与DNA结合的蛋白。 可以测量位于基因组特定区域的不同蛋白质,或特定蛋白在基因组范围内的分布。 该技术的另一个强大应用是分析与转录,有丝分裂或DNA修复等过程相关的组蛋白修饰的变化。

功能&优点:
更快:蛋白G磁珠可在短短一天内完成整个ChIP协议!包含用于处理您的样本的所有试剂-您不′必花费宝贵的时间来制备它们。
更简单:旋转柱使DNA纯化更容易,更可靠-不再进行混乱的苯酚-氯仿提取。
重现性更高:包含阳性和阴性对照抗体和PCR引物,以帮助验证结果并排除实验故障。

应用

用于检测/量化:蛋白G

包装

试剂盒容量:22个染色质免疫沉淀试验

外形

两个盒子包含进行22次独立的染色质免疫沉淀(ChIP)反应所需的所有试剂。 提供的缓冲液足以从多达五个15 cm平板的培养细胞上产生染色质,每个平板可提供多达10个染色质制剂(随细胞和测定类型的不同而不同)。

制备说明

收到后,将组件储存在标签上指示的温度下。当按照指示储存时,试剂盒组件自运输之日起可稳定储存1年。

其他说明

蛋白G磁珠

ChIP稀释缓冲液

低盐清洗缓冲液

高盐清洗缓冲液

LiCl清洗缓冲液

TE缓冲液

细胞裂解缓冲液

核裂解缓冲液

ChIP洗脱缓冲液(含/不含蛋白酶K)

10X甘氨酸

10X PBS

蛋白酶抑制剂混合物II

蛋白酶 K

对照引物

抗-RNA聚合酶II

正常小鼠IgG

旋转过滤器

收集管

结合试剂A

洗涤试剂B

洗脱试剂C

法律信息

MAGNA CHIP is a registered trademark of Merck KGaA, Darmstadt, Germany

免责声明

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

象形图

FlameExclamation mark

警示用语:

Danger

危险分类

Acute Tox. 4 Oral - Aquatic Chronic 3 - Eye Irrit. 2 - Flam. Liq. 2 - Skin Irrit. 2

储存分类代码

3 - Flammable liquids

闪点(°F)

55.4 °F

闪点(°C)

13 °C

法规信息

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Heat shock factor 1 upregulates transcription of Epstein-Barr Virus nuclear antigen 1 by binding to a heat shock element within the BamHI-Q promoter.
Wang, FW; Wu, XR; Liu, WJ; Liao, YJ; Lin, S; Zong, YS; Zeng, MS; Zeng, YX; Mai, SJ; Xie, D
Virology null
Magdalena M Przybycien-Szymanska et al.
PloS one, 6(10), e26647-e26647 (2011-11-01)
EtOH exposure in male rats increases corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus of the hypothalamus (PVN), a brain region responsible for coordinating stress and anxiety responses. In this study we identified the molecular mechanisms involved in mediating these
ChIP-chip: considerations for the design, analysis, and application of genome-wide chromatin immunoprecipitation experiments.
Buck, Michael J and Lieb, Jason D
Genomics, 83, 349-360 (2004)
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Tang, K; Rubenstein, JL; Tsai, SY; Tsai, MJ
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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."

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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