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HUTR08442

Sigma-Aldrich

MISSION® 3′UTR Lenti GoClone™

Powered by SwitchGear Genomics™, 3′UTR, human, SOX2

Synonym(s):

HUTR

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About This Item

UNSPSC Code:
12352200
NACRES:
NA.51

description

Functional Validation of miRNA Gene Targets

product line

MISSION®

concentration

≥1x105 VP/ml (via p24 assay)

human 3′UTR sequence

ACTTCACATGTCCCAGCACTACCAGAGCGGCCCGGTGCCCGGCACGGCCATTAACGGCACACTGCCCCTCTCACACATGTGAGGGCCGGACAGCGAACTGGAGGGGGGAGAAATTTTCAAAGAAAAACGAGGGAAATGGGAGGGGTGCAAAAGAGGAGAGTAAGAAACAGCATGGAGAAAACCCGGTACGCTCAAAAAGAAAAAGGAAAAAAAAAAATCCCATCACCCACAGCAAATGACAGCTGCAAAAGAGAA (3′UTR sequences are truncated after the first 255 bases)

NCBI accession no.

NM_003106

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... SOX2(6657)

Application

To see more application data, protocols, and vector maps visit www.sigma.com/3utr.

Physical form

200 μL of at least 105 VP/mL (via p24 titering assay) lentiviral particles are provided as frozen stock.

Legal Information

Use of this product is subject to one or more license agreements. For details, please see www.sigmaaldrich.com/missionlicense.
GoClone is a trademark of SwitchGear Genomics
MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany
SwitchGear Genomics is a trademark of SwitchGear Genomics

Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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King Chi Chan et al.
Scientific reports, 5, 9979-9979 (2015-04-22)
Nasopharyngeal carcinoma (NPC) is an EBV-associated epithelial malignancy prevalent in southern China. Presence of treatment-resistant cancer stem cells (CSC) may associate with tumor relapse and metastasis in NPC. ICG-001 is a specific CBP/β-catenin antagonist that can block CBP/β-catenin-mediated transcription of
Juan Qin et al.
Oncotarget, 6(9), 6944-6958 (2015-03-10)
Side population (SP) contains cancer stem-like cells (CSLCs). In this study, we characterized SP cells from nasopharyngeal carcinoma (NPC) cell lines and found that SP cells had a higher self-renewal ability in vitro and greater tumorigenicity in vivo. The AKT

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