αcd133 v2lhs 71816

Manufactured by Thermo Fisher Scientific

The αCD133 (V2LHS_71816) is a lab equipment product from Thermo Fisher Scientific. It is a specific antibody targeting the CD133 antigen. The core function of this product is to facilitate the identification and isolation of CD133-positive cells through various research and experimental applications.

Automatically generated - may contain errors

Lab products found in correlation

Lentiviral shrna pgipz vectors ns rhs4348, by Thermo Fisher Scientific (2 mentions) Ex neg m02, by GeneCopoeia (2 mentions) Ex z0396 m02, by GeneCopoeia (1 mentions)

2 protocols using αcd133 v2lhs 71816

CD133 Expression Plasmid and shRNA

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Human cDNA CD133 expression plasmid (EX-Z0396-M02) and empty vector plasmid (EX-NEG-M02) were obtained from GeneCopoeia. Lentiviral shRNA pGIPZ vectors; NS (RHS4348) and αCD133 (V2LHS_71816) were obtained from Thermo Scientific. IKK (IKK-2 S177E S191E) and IKBα (pBabe-Puro-IKBalpha-mut (superrepressor)) plasmids were obtained from Addgene.

Nomura A., Banerjee S., Chugh R., Dudeja V., Yamamoto M., Vickers S.M, & Saluja A.K. (2015). CD133 initiates tumors, induces epithelial-mesenchymal transition and increases metastasis in pancreatic cancer. Oncotarget, 6(10), 8313-8322.

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Modulating NF-κB Activity in Cells

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Human cDNA empty vector plasmid (EX-NEG-M02) and CD133 expression plasmid (EX-Z0396-M02) were attained from GeneCopoeia. Lentiviral shRNA pGIPZ vectors; NS (RHS4348) and αCD133 (V2LHS_71816) were acquired from Thermo Scientific. NF-kB activity was inhibited after transfecting cells with pBabe-puro-IKBalphamut suprerepressor (a gift from William Hahn [ Addgene plasmid#15291]. In this plasmid, the IκBα is mutated at S32A, which keeps NF-κB pathway constitutively repressed (33 (link)).

Nomura A., Gupta V.K., Dauer P., Sharma N.S., Dudeja V., Merchant N., Saluja A.K, & Banerjee S. (2017). NFkB-mediated Invasiveness in CD133+ Pancreatic TICs is Regulated by Autocrine and Paracrine Activation of IL-1 Signaling. Molecular cancer research : MCR, 16(1), 162-172.

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