科技服务 > PCR芯片实验服务 > Gast胃癌体细胞突变PCR 芯片 ric Cancer Mutation PCR Array

Gast胃癌体细胞突变PCR 芯片 ric Cancer Mutation PCR Array

Gast胃癌体细胞突变PCR 芯片ric Cancer Mutation PCR Array
运费 ¥0.00
(库存 9999 件)
qBiomarker Somatic Mutation PCR Array: Human Gastric Cancerhttp://www.sabiosciences.com/images/PriceandOrder.gif
The Human Gastric Cancer qBiomarker Somatic Mutation PCR Array is a translational research tool that allows rapid, accurate and comprehensive profiling of the somatic mutations in human gastric cancer samples in the following key genes: APC, BRAF, CDH1, CDKN2A, CTNNB1, ERBB2, FBXW7, HRAS, KRAS, NRAS, PDGFRA, PIK3CA and P53. These mutations warrant extensive investigation to enhance the understanding of carcinogenesis and identify potential drug targets. The utility of individual and multiple somatic mutation status information in identifying key signaling transduction disruptions has been demonstrated in numerous research studies. For example, the mutation status of the EGFR and KRAS genes can predict the physiological response to certain drugs targeting these molecules. The Human Gastric Cancer qBiomarker Somatic Mutation PCR Array, with its comprehensive content coverage, is designed for studying mutations in the context of cancer and has the potential for discovering and verifying drug target biomarkers for this cancer type and other cancer types in which these mutations were identified. This array includes 81 DNA sequence mutation assays designed to detect the most frequent, functionally verified, and biologically significant mutations in human cancer. These mutations were chosen from curated, comprehensive somatic mutation databases and peer-reviewed scientific literature, and represent the most frequently recurring somatic mutations compiled from over 2000 gastric cancer samples. The simplicity of the product format and operating procedure allows routine somatic mutation profiling in any research laboratory with access to real-time PCR instruments.



APC: 4 Assays
The most commonly detected APC inactivation mutations are mainly composed of truncation mutations (due to nonsense mutations and frameshift mutations) and point mutations between codons 1250 and 1578.
BRAF: 2 Assays
There are two major classes of BRAF mutations. One class leads to increased BRAF kinase activity, such as the p. V600E mutation. The other class leads to impaired kinase activity, such as the p.G469A mutation.
CDH1: 1 Assay
The top CDH1 mutations either are missense mutations or frameshift mutations that lead to C-terminal truncation and secreted E-cadherin fragments.
CDKN2A: 1 Assay
The top CDKN2A loss-of-function mutations occur in the consensus ankyrin domain, which leads to inability to form stable complexes with its targets.
CTNNB1: 18 Assays
The most frequently detected CTNNB1/beta-catenin mutations result in abnormal signaling in the WNT signaling pathway. The mutated codons are mainly several serine/threonine residues targeted for phosphorylation by GSK-3beta.
ERBB2: 2 Assays
The most frequently identified ERBB2 activating mutations cluster in the ERBB2 kinase domain region.
FBXW7: 1 Assay
Typically detected mutations lay in either the third or fourth repeat of the protein's WD40 domain, typically involved in protein-protein interactions.
HRAS: 1 Assay
The most important HRAS mutation in gastric cancer occurs at codon 12.
KRAS: 10 Assays
The mutation assays include the most frequently occurring mutations in KRAS codons 12, 13, and 61. Mutations at these positions result in reduced intrinsic GTPase activity and/or cause KRAS to become unresponsive to RasGAP.
NRAS: 1 Assay
The most important NRAS mutation in gastric cancer occurs at codon 13.
PDGFRA: 1 Assay
The most frequently identified PDGFRA gain-of-function mutations include deletion, point mutation, and deletion-insertion mutations in regions p.D842-S847 and p.R554-E571 as well as the point mutations p.N659Y and p.T674I.
PIK3CA: 4 Assays
The most frequently occurring PIK3CA mutations mainly belong to two classes: gain-of-function kinase domain activating mutations and helical domain mutations that mimic activation by growth factors.
TP53: 35 Assays
The most frequently detected somatic mutations in TP53 are largely composed of DNA-binding domain mutations which disrupt either DNA binding or protein structure.


姓名
电话号码
电子邮箱
公司名称
地址
留言*
 
验证码
提交
我是混淆代码

如果您的浏览器未跳转,请点击此处进行游戏并领取优惠

技术支持 AI智能站群 luis888.vip@gmail.com