pEF1alpha-IRES Vector

Description

pEF1alpha-IRES is a bicistronic mammalian expression vector that allows simultaneous, constitutive expression of two genes of interest from the same mRNA transcript, even after stable integration of the vector into the host cell genome. Stable, constitutive expression of the bicistronic transcript is driven by the human elongation factor 1 alpha EF1alpha promoter, allowing the investigation of a variety of cellular processes such as differentiation in primary or stem cells without the transgene silencing associated with CMV promoters. Our products are to be used forResearch Use Only. They may not be used for any other purpose, including, but not limited to, use in humans, therapeutic or diagnostic use, or commercial use of any kind. Our products may not be transferred to third parties, resold, modified for resale, or used to manufacture commercial products or to provide a service to third parties without our prior written approval. Back Map schematic of the plasmid choices that are available carrying the EF1-alpha promoter.IRES: internal ribosome entry sequence; FP1: fluorescent protein AcGFP1, DsRed-Monomer, or mCherry ; FP2: fluorescent protein mCherry or ZsGreen1 ; MCS: multiple cloning site. Back Expression of AcGFP1 driven by the EF-1 alpha promoter in stem cell lines is higher than expression driven by the CMV promoter.The mouse embryonic stem cell lines E14 Panel A and D3 Panel B were transduced by Lenti-X lentivirus, expressing AcGFP1 either under the control of the CMV promoter or the Elongation factor alpha EF-1 alpha promoter. The expression level of AcGFP1 in infected cells five days postinfection was monitored by FACS analysis using the FL1 channel. The expression of AcGFP1 driven by the EF-1 alpha promoter in both stem cell lines was considerably higher compared to the CMV promoter. This is mainly due to a considerably lower rate of silencing of the EF-1 alpha promoter in stem cells compared to the CMV promoter as published Wang, et al. 2008 Stem Cells Dev17:279289 . Back