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OGS97

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PSF-CMV-EMCV - CMV IRES PLASMID

plasmid vector for molecular cloning

Synonym(e):

cloning vector, expression vector, molecular cloning vector, plasmid, plasmid vector, snapfast vector, vector

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About This Item

UNSPSC-Code:
12352200
NACRES:
NA.85

Form

buffered aqueous solution

Mol-Gew.

size 4761 bp

Bakterienauswahl

kanamycin

Replikationsursprung

pUC (500 copies)

Peptidspaltung

no cleavage

Promotor

Promoter name: CMV
Promoter activity: constitutive
Promoter type: mammalian

Reportergen

none

Versandbedingung

ambient

Lagertemp.

−20°C

Allgemeine Beschreibung

This vector contains the internal ribosome entry site (IRES) from Encephalomyocarditis virus (EMCV) between the promoter and the multiple cloning site (MCS). It is designed to be used to express genes using cap-independent expression systems although the mRNAs produced from this vector contain a 5 prime cap. This vector is not designed for the expression of two proteins from the same mRNA. For this purpose we have designed pSF-CMV-EMCV-PciI where the PciI site contains start codons in the correct position for the IRES to express efficiently. In this vector there is an NcoI site (which contains an ATG start codon) in the correct position to enable efficient expression of a gene in the MCS. We have also developed this same vector with the T7 promoter upstream of the IRES to allow the expression of genes using T7 eukaryotic systems.

Promoter Expression Level: This plasmid contains the mammalian CMV promoter to drive gene expression. We have tested all of our mammalian promoters in a range of cell types and CMV is consistently the strongest in those we have studied. However there are many reports of the CMV promoter demonstrating silencing by methylation in long-term culture.

Anwendung

Cloning in a gene: There is start codon within the NcoI restriction site that is positioned to allow efficient expression from the EMCV IRES. The main MCS for gene insertions in this vector therefore extends from the NcoI restriction site to the XbaI restriction site. The downstream sites (ClaI to NheI sites) have alternate functions and are used to insert other DNA sequences that we sell however they can be used to insert a gene if these functions are not required. These functions include adding peptide tags or downstream IRES elements. The BsgI and BseRI restriction sites cleave within the stop codon in the XbaI site and allow the retrospective fusion of coding sequences. These sites are normally only used on genes that we sell in the main multiple cloning site.

Sequenz

To view sequence information for this product, please visit the product page

Hinweis zur Analyse

To view the Certificate of Analysis for this product, please visit www.oxgene.com

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Lagerklassenschlüssel

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Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Alexander C Cerny et al.
PLoS genetics, 11(10), e1005578-e1005578 (2015-10-29)
Recycling of signaling proteins is a common phenomenon in diverse signaling pathways. In photoreceptors of Drosophila, light absorption by rhodopsin triggers a phospholipase Cβ-mediated opening of the ion channels transient receptor potential (TRP) and TRP-like (TRPL) and generates the visual
Diana Romero et al.
Carcinogenesis, 37(1), 18-29 (2015-10-28)
Dickkopf-3 (Dkk-3) is a secreted protein whose expression is downregulated in many types of cancer. Endogenous Dkk-3 is required for formation of acini in 3D cultures of prostate epithelial cells, where it inhibits transforming growth factor (TGF)-β/Smad signaling. Here, we
Geoffrey M Lynn et al.
Nature biotechnology, 33(11), 1201-1210 (2015-10-27)
The efficacy of vaccine adjuvants such as Toll-like receptor agonists (TLRa) can be improved through formulation and delivery approaches. Here, we attached small molecule TLR-7/8a to polymer scaffolds (polymer-TLR-7/8a) and evaluated how different physicochemical properties of the TLR-7/8a and polymer
Jin-Gyoung Jung et al.
PLoS genetics, 10(10), e1004751-e1004751 (2014-10-31)
The Notch3 signaling pathway is thought to play a critical role in cancer development, as evidenced by the Notch3 amplification and rearrangement observed in human cancers. However, the molecular mechanism by which Notch3 signaling contributes to tumorigenesis is largely unknown.

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