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SHC001

Sigma-Aldrich

MISSION® pLKO.1-puro Empty Vector Control Plasmid DNA

Contains no shRNA insert

Synonym(s):

MISSION® Control Vectors

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About This Item

MDL number:
UNSPSC Code:
41106609
NACRES:
NA.51

product line

MISSION®

concentration

500 ng/μL in TE buffer; DNA (10μg of plasmid DNA)

shipped in

dry ice

storage temp.

−20°C

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General description

The MISSION pLKO.1-puro Control Vector is a lentivirus plasmid vector. The vector does not contain an shRNA insert and is useful as a negative control in experiments using the MISSION shRNA library clones. This allows one to examine the effect of transfection on gene expression and interpret the knockdown effect seen with shRNA clones. Ampicillin and puromycin antibiotic resistance genes provide selection in bacterial or mammalian cells respectively. In addition, self-inactivating replication incompetent viral particles can be produced in packaging cells (HEK293T) by co-transfection with compatible packaging plasmids. The pLKO.1-puro Control Vector is provided as 10 μg of plasmid DNA in Tris-EDTA (TE) buffer at a concentration of 500 ng/μl.

Application

MISSION® pLKO.1-puro Empty Vector Control Plasmid DNA has been used to synthesize and clone shRNAs (which target murine cluster of differentiation 36 (CD36), to generate lentiviral expression vectors.
To see more application data, protocols, vector maps visit sigma.com/shrna.

Legal Information

Use of this product is subject to one or more license agreements. For details, please see http://sigmaaldrich.com/missionlicense.
MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Cardiospecific CD36 suppression by lentivirus-mediated RNA interference prevents cardiac hypertrophy and systolic dysfunction in high-fat-diet induced obese mice.
Zhang Y
Cardiovascular Diabetology, 14 (2015)
AMP-activated protein kinase (AMPK)-induced preconditioning in primary cortical neurons involves activation of MCL-1.
Anilkumar U
Journal of Neurochemistry, 124 (2013)
Gregory J Baker et al.
Cancer research, 74(18), 5079-5090 (2014-07-20)
Natural killer (NK) cells safeguard against early tumor formation by destroying transformed target cells in a process referred to as NK immune surveillance. However, the immune escape mechanisms used by malignant brain tumors to subvert this innate type of immune
Yu Fujita et al.
Cell reports, 24(12), 3296-3311 (2018-09-21)
Inflammatory bowel disease (IBD) is prevalent, but the mechanisms underlying disease development remain elusive. We identify a role for the E3 ubiquitin ligase RNF5 in IBD. Intestinal epithelial cells (IECs) express a high level of RNF5, while the colon of
Timothy Andrew Couttas et al.
Metabolites, 10(6) (2020-06-12)
The number, position, and configuration of double bonds in lipids affect membrane fluidity and the recruitment of signaling proteins. Studies on mammalian sphingolipids have focused on those with a saturated sphinganine or mono-unsaturated sphingosine long chain base. Using high-resolution liquid

Articles

When shRNA is delivered using lentiviral vectors, the sequence encoding the shRNA is integrated into the genome and the knockdown effect is passed on to daughter cells, continuing gene silencing.

When shRNA is delivered using lentiviral vectors, the sequence encoding the shRNA is integrated into the genome and the knockdown effect is passed on to daughter cells, continuing gene silencing.

When shRNA is delivered using lentiviral vectors, the sequence encoding the shRNA is integrated into the genome and the knockdown effect is passed on to daughter cells, continuing gene silencing.

When shRNA is delivered using lentiviral vectors, the sequence encoding the shRNA is integrated into the genome and the knockdown effect is passed on to daughter cells, continuing gene silencing.

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