SignalSilence® β-Arrestin 1 siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit β-arrestin 1 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 β-Arrestin 1 siRNA I 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
Arrestin proteins function as negative regulators of G protein coupled receptor (GPCR) signaling. Cognate ligand binding stimulates GPCR phosphorylation, which is followed by binding of arrestin to the phosphorylated GPCR and the eventual internalization of the receptor and desensitization of GPCR signaling (1). Four distinct mammalian arrestin proteins are known. Arrestin 1 (also known as S-arrestin) and arrestin 4 (or X-arrestin) are localized to retinal rods and cones, respectively. Arrestin 2 (also known as β-arrestin 1) and arrestin 3 (or β-arrestin 2) are ubiquitously expressed and bind to most GPCRs (2). β-arrestin proteins function as adapters and scaffold proteins and play important roles in other processes, such as recruiting c-Src family proteins to GPCRs in ERK activation pathways (3,4). β-arrestins are also involved in some receptor tyrosine kinase signaling pathways (5-8). Additional evidence suggests that β-arrestin proteins translocate to the nucleus and help regulate transcription by binding transcriptional cofactors (9,10).