IGF1R qPCR Primer Pairs, Human

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IGF1R qPCR Primer Pairs, Human: 一般情報

遺伝子情報
種:
Human
NCBI 参考シーケンス番号:
産物のサイズ:
117bp
製品情報
オリゴヌクレオチドの種類:
qPCR Primers
成分:
1 vial of lyophilized qPCR primer mix (1 nmol each primer, sufficient for 200 numbers of 25 μl reactions).
QPCRプライマーの説明:
Verified forward and reverse primers for analyzing the quantitative expression of gene.
アプリケーション & 品質管理
アプリケーション:
SYBR® Green-based quantitative real-time PCR (qPCR).
品質管理:
The primer mix has been verified to generate satisfactory qPCR data on Roche Applied-science LightCycler® 480 Ⅱ.
保存 & 配送
配送方法:
Lyophilized qPCR primer mix is shipped at ambiente temperatura
保存条件:
The lyophilized product is stable for one year from date of receipt when stored at -20℃. The suspended product is stable for six months from date of receipt when stored at -20℃.
***Sino biological qEASY qPCR primer pairs are used for SYBR Green-based real-time RT-PCR, The primers are designed by using SBI's proprietary primer design algorithm. Our primer collection covers the entire human genomes. It can be widely applied in the quantitative analysis of gene expression.***

特徴とメリット

独特なプライマー設計

ゲノムDNAの増幅を効果的に回避するために、このプライマーペアには少なくとも1つのプライマーまたは産物がイントロンを横切るように、特定の遺伝子の異なる変異体の保存領域でプライマーを設計します。

厳格なスクリーニング検証プロセス

プラスミド標準品でqPCRプライマーの感度、増幅効率、および特異性をスクリーニングし、陽性組織または細胞で検証し確認します。

均一なPCR条件、操作が簡単で、時間とコストを節約します

~100%という増幅効率で、RNA定量の正確さを保証

IGF1R qPCR Primer Pairs, Human: 検証済の画像

IGF1R dissolution curves
IGF1R amplification curves

IGF1R qPCR Primer Pairs, Human: 別名

CD221 qPCR Primer Pairs, Human; IGF-I R qPCR Primer Pairs, Human; IGF1 Receptor qPCR Primer Pairs, Human; IGFIR qPCR Primer Pairs, Human; IGFR qPCR Primer Pairs, Human; JTK13 qPCR Primer Pairs, Human

IGF1R 背景情報

The insulin-like growth factor-1 receptor (IGF1R) is a transmembrane tyrosine kinase involved in several biological processes including cell proliferation, differentiation, DNA repair, and cell survival. This a disulfide-linked heterotetrameric transmembrane protein consisting of two α and two β subunits, and among which, the α subunit is extracellular while the β subunit has an extracellular domain, a transmembrane domain and a cytoplasmic tyrosine kinase domain. IGF1R signalling pathway is activated in the mammalian nervous system from early developmental stages. Its major effect on developing neural cells is to promote their growth and survival. This pathway can integrate its action with signalling pathways of growth and morphogenetic factors that induce cell fate specification and selective expansion of specified neural cell subsets. Modulation of cell migration is another possible role that IGF1R activation may play in neurogenesis. In the mature brain, IGF-I binding sites have been found in different regions of the brain, and multiple reports confirmed a strong neuroprotective action of the IGF-IR against different pro-apoptotic insults. IGF1R is an important signaling molecule in cancer cells and plays an essential role in the establishment and maintenance of the transformed phenotype. Inhibition of IGF1R signaling thus appears to be a promising strategy to interfere with the growth and survival of cancer cells. IGF1R is frequently overexpressed by tumours, and mediates proliferation and apoptosis protection. IGF signalling also influences hypoxia signalling, protease secretion, tumour cell motility and adhesion, and thus can affect the propensity for invasion and metastasis. Therefore, the IGF1R is now an attractive anti-cancer treatment target.
完全な名称
insulin-like growth factor 1 receptor
参考文献
  • Bhr C, et al. (2004) The insulin like growth factor-1 receptor (IGF-1R) as a drug target: novel approaches to cancer therapy. Growth Horm IGF Res. 14 (4): 287-95.
  • Riedemann J, et al. (2006) IGF1R signalling and its inhibition. Endocr Relat Cancer. 13 Suppl 1: 33-43.
  • Gualco E, et al. (2009) IGF-IR in neuroprotection and brain tumors. Front Biosci. 14: 352-75.
  • Annenkov A. (2009) The insulin-like growth factor (IGF) receptor type 1 (IGF1R) as an essential component of the signalling network regulating neurogenesis. Mol Neurobiol. 40 (3): 195-215.
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