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OGS43

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PSF-EF1 ALPHA - ELONGATION FACTOR ALPHA PROMOTER 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 4872 bp

Bakterienauswahl

kanamycin

Replikationsursprung

pUC (500 copies)

Peptidspaltung

no cleavage

Promoter

Promoter name: EF1-alpha
Promoter activity: constitutive
Promoter type: mammalian

Reportergen

none

Versandbedingung

ambient

Lagertemp.

−20°C

Allgemeine Beschreibung

PSF-EF1 ALPHA - ELONGATION FACTOR ALPHA PROMOTER PLASMID contains the EF1 α promoter upstream of the multiple cloning site (MCS) for expression in mammalian cells. Transcription termination is mediated by the SV40 poly-adenylation signals downstream of the MCS.

Anwendung

Cloning in a gene: This plasmid has been designed to be compatible with a range of cloning techniques. The multiple cloning site contains a range of standard commonly used restriction sites for cloning. Using these sites genes can be inserted using standard cloning methods with DNA ligase. Other methods such as ligase independent cloning (LIC) Gibson Assembly InFusionHD or Seamless GeneArt can also be used and because all of our plasmids are based on the same backbone the same method can be used for cloning into all of our catalogue vectors.

Multiple cloning site notes: There are a few important sites within the MCS. These include the NcoI site the XbaI site and the BsgI and BseRI sites. The NcoI site contains a start codon that is immediately downstream of both a Kozak and Shine-Dalgarno ribosomal binding site. These allow for optimal positioning of genes when the start codon is placed in this location. If this is not required and you wish to use a downstream site for gene cloning you can remove the NcoI site by cleaving the plasmid with KpnI.

The XbaI site contains a stop codon. This stop codon is positioned in a specific position in relation to the BsgI and BseRI sites that are immediately downstream. When either BseRI or BsgI cleave the plasmid they produce a TA overhang from the stop codon in the XbaI site that is compatible with all of our peptide tag plasmids cut with the same sites. BseRI and BsgI sites are non-palindromic and cleave a defined number of bases away from their binding site.

Whenever we clone a gene into our multiple cloning site we always position the start and stop codon in the same positions in the MCS. If the start and ends of the genes are not compatible with NcoI and XbaI we extend the sequence to the nearest external sites but keep the start and stop codons locations consistent.

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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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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