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SHC004

Sigma-Aldrich

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

shRNA sequence targeting tGFP

Sinónimos:

MISSION® Control Vectors

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1 PKG
$370.80

$370.80

Precio de catálogo$412.00Ahorre 10 %

Fecha estimada de envío13 de abril de 2025

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1 PKG
$370.80

About This Item

MDL number:
MFCD07785395
UNSPSC Code:
41106609
NACRES:
NA.51

$370.80

Precio de catálogo$412.00Ahorre 10 %

Fecha estimada de envío13 de abril de 2025

Solicitar un pedido a granelSolicitar más información

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.[1] 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.[2][3] 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.[4][5][6]
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.

Optional

Referencia del producto
Descripción
Precios

SHC002

MISSION® pLKO.1-puro Non-Mammalian shRNA Control Plasmid DNA, Targets no known mammalian genes

SHC001V

MISSION® pLKO.1-puro Empty Vector Control Transduction Particles, Contains no shRNA insert

SHC003

MISSION® pLKO.1-puro-CMV-TurboGFP™ Positive Control Plasmid DNA, Green fluorescent protein marker to monitor transduction efficiency

SHC002V

MISSION® pLKO.1-puro Non-Mammalian shRNA Control Transduction Particles, Targets no known mammalian genes

SHC003V

MISSION® pLKO.1-puro-CMV-TurboGFP™ Positive Control Transduction Particles, Green fluorescent protein marker to monitor transduction efficiency

SHC004V

Partículas de control de transducción de shRNA MISIÓN® pLKO.1-puro TurboGFP™, shRNA sequence targeting tGFP

SHM01

ExpressMag® Super Magnetic Kit, Increases transduction efficiency

SHM02

ExpressMag® 96-Well Magnetic Kit, Increases transduction efficiency

Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

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Blocking Hedgehog release from pancreatic cancer cells increases paracrine signaling potency.
Damhofer H, et al.
Journal of Cell Science, 128(1), 129-139 (2015)
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)
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
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
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