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About This Item
NACRES:
NA.51
UNSPSC Code:
41106609
Product Name
MISSION® pLKO.1-puro Non-Target shRNA Control Transduction Particles, High Titer, Targets no known genes from any species
product line
MISSION®
concentration
≥1x109 VP/ml (via p24 assay)
shipped in
dry ice
storage temp.
−70°C
Quality Level
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Application
To see more application data, protocols, vector maps visit sigma.com/shrna.
General description
The MISSION pLKO.1-puro Non-Target shRNA Control Transduction Particles, High Titer contain an shRNA insert that does not target any known genes from any species, making it useful as a negative control in experiments using the MISSION shRNA library clones. This allows one to examine the effect of transduction of a short-hairpin 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.
High titer virus is useful when performing in vivo research.
High titer virus is useful when performing in vivo research.
When conducting experiments using MISSION® shRNA clones, the proper controls should be a key element of your experimental design to allow for accurate interpretation of knockdown results. The MISSION Control Transduction Particles are a critical positive control to monitor transduction efficiency.
To see more application data, protocols, vector maps visit sigma.com/shrna.
To see more application data, protocols, vector maps visit sigma.com/shrna.
Legal Information
MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class
12 - Non Combustible Liquids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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Najim Lahrouchi et al.
Nature communications, 10(1), 1180-1180 (2019-03-14)
A failure in optic fissure fusion during development can lead to blinding malformations of the eye. Here, we report a syndrome characterized by facial dysmorphism, colobomatous microphthalmia, ptosis and syndactyly with or without nephropathy, associated with homozygous frameshift mutations in
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