SignalSilence® FoxO1 siRNA II 能够抑制人和小鼠FoxO1的表达。来自Cell Signaling Technology (CST)的SignalSilence®FoxO1 siRNA II 可以帮助研究者通过RNA干扰特异性地抑制FoxO1的表达,这种方法可以通过将双链RNA分子传递到细胞内从而使基因表达有选择的沉默。来自CST的所有的SignalSilence®siRNA产品都是经过内部严格检测的,并且通过Western blot 分析证明确实能够减少目的蛋白的表达。通过三苯甲基分析每个碱基以监测寡核苷酸的合成,确保合适的配对效率。随后寡核苷酸通过亲和固相萃取法纯化。退火的RNA双链通过质谱分析来证实其精确的组成。每一批产品都通过质谱分析与前面的产品进行比较,来保证不同批次之间的最大一致性。CST推荐使用100 nM SignalSilence®FoxO1 siRNA II 进行转染,48到72小时后对细胞进行裂解。转染步骤按照转染试剂说明书提供的步骤进行。遇到任何使用方面的问题,请随时联系CST。Forkhead转录因子家族参与横纹肌肉瘤和急性白血病的发生(1-3)。在这个家族中,三个成员(FoxO1,FoxO4和FoxO3a)与线虫的同源基因DAF-16具有序列相似度,而DAF-16介导包括IGFR1,PI3K和Akt在内的信号通路(4-6)。活化的forkhead成员作为肿瘤抑制因子,促进细胞周期阻滞和凋亡。FOXO家族任何成员的表达上调都会激活细胞周期抑制剂p27 Kip1。Forkhead转录因子也参与TGF-β介导的p21 CIP1上调,而这个上调过程可以被PI3K负调控(7)。forkhead转录因子被Akt在Thr24,Ser256以及Ser319磷酸化后而失活,导致出核转运与转录因子活性的抑制(8),最终导致增殖上调。Forkhead转录因子活性也可以被去乙酰化酶sirtuin(SirT1)抑制(9)。
Species predicted to react based on 100% sequence homology:Mouse
Specificity / Sensitivity
SignalSilence® FoxO1 siRNA II will inhibit human and mouse FoxO1 expression.
Description
SignalSilence® FoxO1 siRNA II from Cell Signaling Technology (CST) allows the researcher to specifically inhibit FoxO1 expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence® siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis.
Quality Control
Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
Directions for Use
CST recommends transfection with 100 nM FoxO1 siRNA II 48 to 72 hours prior to cell lysis. For transfection procedure, follow protocol provided by the transfection reagent manufacturer. Please feel free to contact CST with any questions on use.
Background
The Forkhead family of transcription factors is involved in tumorigenesis of rhabdomyosarcoma and acute leukemias (1-3). Within the family, three members (FoxO1, FoxO4, and FoxO3a) have sequence similarity to the nematode orthologue DAF-16, which mediates signaling via a pathway involving IGFR1, PI3K, and Akt (4-6). Active forkhead members act as tumor suppressors by promoting cell cycle arrest and apoptosis. Increased expression of any FoxO member results in the activation of the cell cycle inhibitor p27 Kip1. Forkhead transcription factors also play a part in TGF-β-mediated upregulation of p21 Cip1, a process negatively regulated through PI3K (7). Increased proliferation results when forkhead transcription factors are inactivated through phosphorylation by Akt at Thr24, Ser256, and Ser319, which results in nuclear export and inhibition of transcription factor activity (8). Forkhead transcription factors can also be inhibited by the deacetylase sirtuin (SirT1) (9).