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PSF-CMV-NH2-V5-EKT-NCOI - N-TERMINAL V5 TAG PLASMID

plasmid vector for molecular cloning

Synonyme(s) :

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

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About This Item

Code UNSPSC :
12352200
Nomenclature NACRES :
NA.85

Étiquette/Marqueur

V5 tagged

Forme

buffered aqueous solution

Poids mol.

size 4280 bp

Sélection de bactéries

kanamycin

Origine de la réplication

pUC (500 copies)

Clivage des peptides

no cleavage

Localisation du marqueur peptidique

N-terminal

Promoteur

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

Gène reporter

none

Conditions d'expédition

ambient

Température de stockage

−20°C

Description générale

Plasmid vector adds a V5 epitope tag to the N-terminus of a protein that is encoded within the multiple cloning site. This tag allows the detection and purification of a tagged protein using antibodies raised against the Influenza V5 epitope. The V5 tag coding sequence is GKPIPNPLLGLDST. There is an enterokinase cleavage site (DDDDK) immediately downstream of the V5 tag that can be used to remove the V5 tag from a purified protein. It cleaves after the lysine residue.

Promoter Expression Level: PSF-CMV-NH2-V5-EKT-NCOI - N-terminal V5 tag 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.

Application

Molecular cloning vector has been designed to allow the addition of a peptide tag to the end of a protein of interest using standard cloning techniques.Multiple Cloning Site Notes:

There is a start codon in the NcoI site can be removed by digestion with KpnI if required. The MCS for gene insertions extends from NotI to XbaI however the tag resides between the NotI and HindIII sites. There are Shine-Dalgarno sequences and KOZAK sequences aligned with the start codon of the peptide tag.

The ClaI to NheI sites have other functions such as adding C-terminal peptide tags second promoters or IRES expression components. The BsgI and BseRI restriction sites cleave within the stop codon in the XbaI site and allow the retrospective fusion of C-terminal peptide tags sequences if the stop codon is placed in this position.

Séquence

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

Remarque sur l'analyse

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

Produit(s) apparenté(s)

Réf. du produit
Description
Tarif

Code de la classe de stockage

12 - Non Combustible Liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

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
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
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
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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