人癌症药物靶标ChIP qPCR芯片 Cancer Drug Targets EpiTect ChIP qPCR Array

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Cancer Drug Targets EpiTect ChIP qPCR Array

人癌症药物靶标ChIP qPCR芯片
 

Product	Species	Technology	Cat. No.
Cancer Drug Targets EpiTect ChIP qPCR Array	Human	Histone Modifications	GH-507A
Cancer Drug Targets EpiTect ChIP qPCR Array	Mouse	Histone Modifications	GM-507A

The Human Cancer Drug Targets EpiTect Chip qPCR Array profiles the histone modification status or “histone code” of 84 actively sought targets for anticancer therapeutics and drug development. Histone modifications define chromatin structure, and some correlate closely with the transcriptional activity of associated genes.In vitro screening of therapeutics for a given cancer type increasingly depends on not only the activity, but also the expression and epigenetic status of oncogenes. For example, histone deacetylase (HDAC) inhibitors induce tumor suppressor gene expression, slowing growth and proliferation, but could also increase oncogene expression. The choice to add HDAC inhibitors to a drug regimen can depend on the histone codes of the two gene classes. Cancer cells with oncogenes in a heterochromatin state may respond better to HDAC inhibitor treatment because these genes would not be expressed or easily induced. Comprehensively understanding how oncogenes contribute to tumor growth and survival on the molecular level requires a determination of the epigenetic mechanisms regulating their expression. Using chromatin immunoprecipitation and this real-time PCR Array, you can easily and reliably analyze the histone modification patterns associated with a focused panel of important cancer-related genes.
 
 
人癌症药物靶标ChIP qPCR芯片用于分析疗法和药物开发积极寻求的84个靶标的组蛋白修饰状态或组蛋白密码。组蛋白修饰调节染色质结构和与转录活性相关的基因。体外筛选癌症疗法对于一个给定的类型不仅越来越多地依赖于活性，还依赖致癌基因的表达和表观遗传状态。例如组蛋白脱乙酰酶(HDAC)YZ剂引起肿瘤YZ基因表达，生长和增殖减缓，但也可能增加致癌基因表达。可以根据两类组蛋白编码基因，选择添加HDACYZ剂到给YF案。癌细胞在癌基因异染色质状态下可能对HDACYZ剂ZL反应更好，因为这些基因不表达或容易诱导。全面了解致癌基因在分子水平上促进肿瘤的生长和生存需要一个确定的调节他们表达的表观遗传机制。通过染色质免疫沉淀和EpiTect ChIP qPCR芯片，可以很简易可靠地分析组蛋白的化学修饰模式与重要癌症相关基因的表达。
 
 
 
Apoptosis:BCL2, BIRC5.
PI-3 Kinases & Phosphatases:FRAP1 (MTOR), PIK3C2A, PIK3C3, PIK3CA.
Growth Factors & Receptors:EGFR, ERBB2, ERBB3, ERBB4, FIGF, FLT1, FLT4, IGF1, IGF1R, IGF2, KDR, KIT, PDGFRA, PDGFRB.
Drug Metabolism:ABCC1, GSTP1, PTGS2, TXN, TXNRD1.
G Protein Signaling:RHOA, RHOB.
Hormone Receptors:ESR1, ESR2, PGR.
Heat Shock Proteins:HSP90AA1, HSP90B1.
Receptor Tyrosine Kinase Signaling:AKT1, AKT2, GRB2.
Cathepsins:CTSB, CTSD, CTSL1, CTSS.
Cell Cycle:CDC2, CDC25A, CDK2, CDK4, CDK5, CDK7, CDK8, CDK9, MDM2, MDM4, TERT.
Topoisomerases, Type II:TOP2A, TOP2B.
Transcription Factors:ATF2, HIF1A, IRF5, NFKB1, TP53.
Protein Kinases:AURKA, AURKB, AURKC, PLK1, PLK2, PLK3, PLK4, PRKCA, PRKCB, PRKCD, PRKCE.
RAS Signaling:HRAS, KRAS, NRAS.
Histone Deacetylases:HDAC1, HDAC11, HDAC2, HDAC3, HDAC4, HDAC6, HDAC7, HDAC8.
Poly ADP-Ribose Polymerases:PARP1, PARP2, PARP4, TNKS.
Structural Protein:NTN3.