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pCLXSN Retrovirus Expression Vector

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pCLXSN Retrovirus Expression Vector [NBP2-29500] - Schematic presentation of pCLXSN vector: CMV immediate early enhancer-promoter allows highefficiency transcription in 293 cells. However, this is lost during viral ...read more

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Summary
Concentration
Please see the protocols for proper use of this product. If no protocol is available, contact technical services for assistance.

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Applications/Dilutions

Application Notes
The RetroMax system is designed for maximal virus titer in 293 cells. It takes advantages of two properties of 293 cells, i) high level of transfectibility, ii) strong E1A-mediated stimulation of CMV promoter controlled transcription. 293 cells are of nonmurine origin, hence the problem of selective packaging and transfer of VL30 genomes (present in all murine packaging cells) are avoided. Vector supernatants are free of helper virus and are of sufficiently high titer within 2 days of transient transfection in 293 cells to permit infection of more than 50% of dividing target cells in culture.
For amplification, transform DH-5a or similar bacteria and plate on LB plates containing 50 mg/ml ampicillin.
Publications
Read Publications using NBP2-29500.

Packaging, Storage & Formulations

Storage
Store at -20C. Avoid freeze-thaw cycles.
Buffer
10 ug in 20 ul 1x TE (10 mM Tris, pH 7.5, 1 mM EDTA)
Concentration
Please see the protocols for proper use of this product. If no protocol is available, contact technical services for assistance.

Alternate Names for pCLXSN Retrovirus Expression Vector

  • pCLXSN Retrovirus
  • pCLXSN
  • Retrovirus Expression Vector
  • Retrovirus

Background

The pCLXSN expression vector is a part of the RetroMax expression system and has been designed to maximize recombinant-retrovirus titers in a simple, efficient, and flexible experimental system. All members of the RetroMax expression vector family (pCLXSN, pCLNCX, pCLNRX, and pCLNDX) have an extended packaging signal (omega+) and are derived from safetymodified retrovirus vectors in which the gag open reading frame has been stopped by a point mutation (1), thereby minimizing the opportunity for replication competent retrovirus production by recombination with packaging genome.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Support products are guaranteed for 6 months from date of receipt.
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Publications for pCLXSN Retrovirus Expression Vector (NBP2-29500)(9)


Showing Publications 1 - 9 of 9.
Publications using NBP2-29500 Applications Species
Xu C, Xu W, Palmer AE et al. BI-1 regulates endoplasmic reticulum Ca2+ homeostasis downstream of Bcl-2 family proteins. J Biol Chem. 2008-04-25 [PMID: 18299329]
Hashimoto N, Kiyono T, Wada MR et al. Immortalization of human myogenic progenitor cell clone retaining multipotentiality. Biochem Biophys Res Commun. 2006-10-06 [PMID: 16919240]
Ogawa D, Nomiyama T, Nakamachi T et al. Activation of peroxisome proliferator-activated receptor gamma suppresses telomerase activity in vascular smooth muscle cells. Circ Res. 2006-04-14 [PMID: 16556873]
Zhang W, Hirschler-Laszkiewicz I, Tong Q et al. TRPM2 is an ion channel that modulates hematopoietic cell death through activation of caspases and PARP cleavage. Am J Physiol Cell Physiol. 2006-04-01 [PMID: 16306129]
Bill HM, Knudsen B, Moores SL et al. Epidermal growth factor receptor-dependent regulation of integrin-mediated signaling and cell cycle entry in epithelial cells. Mol Cell Biol. 2004-10-01 [PMID: 15367678]
Zhang Y, Bliska JB. Role of Toll-like receptor signaling in the apoptotic response of macrophages to Yersinia infection. Infect Immun. 2003-03-01 [PMID: 12595470]
Kudoh A, Fujita M, Kiyono T et al. Reactivation of lytic replication from B cells latently infected with Epstein-Barr virus occurs with high S-phase cyclin-dependent kinase activity while inhibiting cellular DNA replication. J Virol. 2003-01-01 [PMID: 12502801]
van Deventer HW, Serody JS, McKinnon KP et al. Transfection of macrophage inflammatory protein 1 alpha into B16 F10 melanoma cells inhibits growth of pulmonary metastases but not subcutaneous tumors. J Immunol. 2002-08-01 [PMID: 12133994]
Boccaccio C, Ando' M, Comoglio PM. A differentiation switch for genetically modified hepatocytes. FASEB J. 2002-01-01 [PMID: 11709498]

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