This pcDNA™3.1/Zeo(+) vector is designed for high-level, constitutive expression in a variety of mammalian cell lines. It contains a Zeocin™ selectable marker and a forward-orientation multiple cloning site.
The pcDNA™3.1 Expression Vector Family Three untagged versions of pcDNA™3.1 (available separately), each with a different selectable marker (Geneticin™, Zeocin™, or Hygromycin), are for use alone or in co-transfections. All three vectors offer the following features: • Cytomegalovirus (CMV) enhancer-promoter for high-level expression • Large multiple cloning site in either forward (+) or reverse (-) orientations • Bovine Growth Hormone (BGH) polyadenylation signal and transcription termination sequence for enhanced mRNA stability • SV40 origin for episomal replication and simple vector rescue in cell lines expressing the large T antigen (i.e., COS-1 and COS-7) • Ampicillin resistance gene and pUC origin for selection and maintenance in E. coli
For Research Use Only. Not for use in diagnostic procedures.
Specifications
Constitutive or Inducible SystemConstitutive
Delivery TypeTransfection
For Use With (Application)Constitutive Expression
Product TypeMammalian Expression Vector
Quantity20 μg
Selection Agent (Eukaryotic)Zeocin™
VectorpcDNA
Cloning MethodRestriction Enzyme/MCS
Product LinepcDNA
PromoterCMV
Protein TagUntagged
Unit Size20 µg
Contents & Storage
20 μg of this pcDNA™3.1/Zeo(+) vector, as well as an expression control, are supplied supercoiled and lyophilized. Store at -20°C. Vectors are guaranteed stable for 6 months when properly stored.
Citations & References (19)
Citations & References
Abstract
A novel N-terminal splice variant of the rat H+-K+-ATPase alpha2 subunit. Cloning, functional expression, and renal adaptive response to chronic hypokalemia.
Authors:Kone BC, Higham SC
Journal:J Biol Chem
PubMed ID:9446555
'The H+-K+-ATPase of renal collecting duct mediates K+ conservation during chronic hypokalemia. K+ deprivation promotes H+-K+-ATPase alpha2 (HKalpha2) gene expression in the medullary collecting duct, the principal site of active K+ reabsorption, suggesting that this isozyme contributes to renal K+ reclamation. We report here that alternative transcriptional initiation and mRNA ... More
An alternative processing of integrin alpha(v) subunit in tumor cells by membrane type-1 matrix metalloproteinase.
Authors: Ratnikov Boris I; Rozanov Dmitri V; Postnova Tanya I; Baciu Peter G; Zhang Heying; DiScipio Richard G; Chestukhina Galina G; Smith Jeffrey W; Deryugina Elena I; Strongin Alex Y;
Journal:J Biol Chem
PubMed ID:11741954
'Membrane type-1 matrix metalloproteinase (MT1-MMP) and alpha(v)beta(3) integrin are both essential to cell invasion. Maturation of integrin pro-alpha(v)chain (pro-alpha(v)) involves its cleavage by proprotein convertases (PC) to form the disulfide-bonded 125-kDa heavy and 25-kDa light alpha chains. Our report presents evidence of an alternative pathway of pro-alpha(v) processing involving MT1-MMP. ... More
Apical sorting of beta-secretase limits amyloid beta-peptide production.
Authors: Capell Anja; Meyn Liane; Fluhrer Regina; Teplow David B; Walter Jochen; Haass Christian;
Journal:J Biol Chem
PubMed ID:11741885
'Polarized cells such as neurons and endothelial cells appear to be involved in two invariant pathological features of Alzheimer''s disease pathology, namely the formation of senile plaques and cerebral amyloid angiopathy. This implicates polarized sorting mechanisms in the production and accumulation of amyloid beta-peptide (Abeta). We have now studied polarized ... More
Cellular response to oncogenic ras involves induction of the Cdk4 and Cdk6 inhibitor p15(INK4b).
Authors:Malumbres M, Perez De Castro I, Hernandez MI, Jimenez M, Corral T, Pellicer A
Journal:Mol Cell Biol
PubMed ID:10733595
'The cell cycle inhibitor p15(INK4b) is frequently inactivated by homozygous deletion together with p16(INK4a) and p19(ARF) in some types of tumors. Although the tumor suppressor capability of p15(INK4b) is still questioned, it has been found to be specifically inactivated by hypermethylation in hematopoietic malignancies in the absence of p16(INK4a) alterations. ... More
Insulin-degrading enzyme rapidly removes the beta-amyloid precursor protein intracellular domain (AICD).
'The intramembranous gamma-secretase cleavage of the beta-amyloid precursor protein (APP) is dependent on biologically active presenilins (PS). Notch also undergoes a similar PS-dependent gamma-secretase-like cleavage, resulting in the liberation of the Notch intracellular domain (NICD), which is critically required for developmental signal transduction. gamma-Secretase processing of APP results in the ... More