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SHC216V

Sigma-Aldrich

MISSION® TRC2 pLKO.5-puro Non-Target shRNA Control Transduction Particles

Targets no known genes from any species

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Synonym(s):
MISSION®, MISSION® Control Transduction Particles, negative control, negative shRNA control, non-target control, non-target shRNA, non-target shRNA control, shRNA control
NACRES:
NA.51

Quality Level

100
200

product line

MISSION®

concentration

≥1x106 VP/ml (via p24 assay)

shipped in

dry ice

storage temp.

−70°C

Related Categories

General description

The MISSION® TRC2 pLKO.5-puro Non-Target shRNA Control Tranduction Particles 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. The Non-Target shRNA Control Transduction Particles are provided as 200 uL at 1 x 106 TU/mL via p24 assay.
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.

Application

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 Code

12 - Non Combustible Liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Small-molecule targeting of signal transducer and activator of transcription (STAT) 3 to treat non-small cell lung cancer.
Lewis KM
Lung Cancer, 90(2), 182-190 (2015)
STAT-3 contributes to pulmonary fibrosis through epithelial injury and fibroblast-myofibroblast differentiation.
Pedroza M
Faseb Journal, 30(1), 129-140 (2016)
The LIN28B/let-7 axis is a novel therapeutic pathway in multiple myeloma.
Manier S
Leukemia, 31(4), 853-860 (2017)
Mesias Pedroza et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 30(1), 129-140 (2015-09-02)
Lung fibrosis is the hallmark of the interstitial lung diseases. Alveolar epithelial cell (AEC) injury is a key step that contributes to a profibrotic microenvironment. Fibroblasts and myofibroblasts subsequently accumulate and deposit excessive extracellular matrix. In addition to TGF-β, the
Curtis A Clark et al.
Cancer research, 76(23), 6964-6974 (2016-09-28)
PD-L1 antibodies produce efficacious clinical responses in diverse human cancers, but the basis for their effects remains unclear, leaving a gap in the understanding of how to rationally leverage therapeutic activity. PD-L1 is widely expressed in tumor cells, but its
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