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SHC014

Sigma-Aldrich

MISSION® pLKO.1-puro-UbC-TurboGFP Positive Control Plasmid DNA

Contains a gene encoding TurboGFP, under the control of the UbC promoter

Synonym(s):

MISSION® Control Vectors

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About This Item

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

Quality Level

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

Ampicillin and puromycin antibiotic resistance genes provide selection in bacterial or mammalian cells respectively. In addition, we recommend producing self-inactivating replication incompetent viral particles in packaging cells (HEK293T) by co-transfection with compatible packaging plasmids. The UbC-TurboGFP Control Vector is provided as 10 μg of plasmid DNA in Tris-EDTA (TE) buffer at a concentration of 500 ng/μl.

Application

To see more application data, protocols, vector maps visit sigma.com/shrna.
Silencing of the CMV promoter can be a problem in some cell types. For these cells, the ubiquitin promoter (UbC) can be a viable alternative. The MISSION UbC-TurboGFP Control Vector is a 9092 base pair lentivirus plasmid vector that contains a gene encoding TurboGFP, under the control of the UbC promoter. The UbC-Turbo-GFP Control Vector is useful as a positive control in experiments using the MISSION shRNA library clones for applications in which an alternate promoter is necessary.

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
TurboGFP is a trademark of Evrogen Co.

Storage Class Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Jun Wu et al.
Cell reports, 33(7), 108395-108395 (2020-11-19)
The mammalian SWitch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling BAF (BRG1/BRM-associated factor) complex plays an essential role in developmental and pathological processes. We show that the deletion of Baf155, which encodes a subunit of the BAF complex, in the Tie2(+) lineage (Baf155 (CKO)

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