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SHC004

Sigma-Aldrich

MISSION® pLKO.1-puro TurboGFP™ shRNA Control Plasmid DNA

shRNA sequence targeting tGFP

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Synonym(s):
MISSION® Control Vectors
MDL number:
MFCD07785395
NACRES:
NA.51

Quality Level

200

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 TurboGFP shRNA Control Vector is a 7,087 base pair lentivirus plasmid vector that contains an shRNA sequence targeting TurboGFP. The TurboGFP shRNA Control Vector is useful as a positive knockdown control in experiments using the MISSION TurboGFP positive control vector or in cell lines expressing TurboGFP. TurboGFP is an improved variant of the green fluorescent protein copGFP cloned from copepoda Pontellina plumata.
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 TurboGFP shRNA 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 TurboGFP™ shRNA control plasmid DNA has been used as lentiviral transduction and RNA interference assay.
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
TurboGFP is a trademark of Evrogen Co.

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SHC003

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SHC003V

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SHC004V

MISSION® pLKO.1-puro TurboGFP™ shRNA Control Transduction Particles, shRNA sequence targeting tGFP

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SHM02

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Regulatory Information

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The MEK2-binding tumor suppressor hDlg is recruited by E-cadherin to the midbody ring
Gaudet S, et al.
BMC Cell Biology, 12(1), 55-55 (2011)
Blocking Hedgehog release from pancreatic cancer cells increases paracrine signaling potency.
Damhofer H, et al.
Journal of Cell Science, 128(1), 129-139 (2015)
Lorraine Springuel et al.
Cellular and molecular life sciences : CMLS, 73(24), 4739-4748 (2016-07-21)
Genomic instability drives cancer progression by promoting genetic abnormalities that allow for the multi-step clonal selection of cells with growth advantages. We previously reported that the IL-9-dependent TS1 cell line sequentially acquired activating substitutions in JAK1 and JAK3 upon successive
SMCHD1 regulates a limited set of gene clusters on autosomal chromosomes
Mason A G, et al.
Skeletal Muscle, 7(1), 12-12 (2017)
Ze-Qiang Ren et al.
Pathology oncology research : POR, 26(2), 1153-1163 (2019-06-09)
Cullin-1 (CUL1) is an important factor for tumor growth and a potential therapeutic target for breast cancer therapy, but the molecular mechanism in triple-negative breast cancer (TNBC) is unknown. In the present study, CUL1 shRNA was transfected into BT549 and
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