CMV Adenoviral Expression System

CMV Adenoviral Expression System
  • Engineered to produce 100- to 10,000-fold fewer wild type plaques than most other expression systems
  • Generate high-titer virus in about 2-3 weeks compared to 2-3 months with other systems
  • Cloning capacity of shuttle vector = 6.9 kb

 

Frequently Asked Questions about this product

General FAQs about using Adenovirus

General FAQs about Viral Gene Delivery

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RAPAd® CMV Adenoviral Expression System
Catalog Number
VPK-252
Size
1 kit
Detection
N/A
Manual/Data Sheet Download
SDS Download
Map Download
Sequence Download
Price
$920.00
Product Details

Making an adenovirus with traditional recombinant methods takes 2-3 months and requires tedious plaque recombination. More recent technologies have shortened this time somewhat, but still produce relatively high amounts of wild type (replication-competent) plaques, levels of which increase with serial amplification.

The RAPAd® Adenoviral Expression Systems produce recombinant adenovirus with substantially reduced wild-type virus, while considerably shortening the production time to 2-3 weeks. Serial amplification of adenovirus produced using the RAPAd® system does not significantly increase replication-competent adenovirus levels. The system uses a backbone vector from which the 5' ITR, packaging signal and E1 sequences have been removed.

Recent Product Citations
  1. Zhang, C. et al. (2023). PIMT is a novel and potent suppressor of endothelial activation. Elife. doi: 10.7554/eLife.85754.
  2. Wade, M. et al. (2021). In vivo generation of collagen specific Tregs with AAV8 suppresses autoimmune responses and arthritis in DBA1 mice through IL10 production. Sci Rep. 11(1):18204. doi: 10.1038/s41598-021-97739-w.
  3. Sun, L. et al. (2020). miR-182-3p/Myadm contribute to pulmonary artery hypertension vascular remodeling via a KLF4/p21-dependent mechanism. Theranostics. 10(12):5581-5599. doi: 10.7150/thno.44687.
  4. Guček, A. et al. (2019). Fusion pore regulation by cAMP/Epac2 controls cargo release during insulin exocytosis. eLife. 8:e41711. doi: 10.7554/eLife.41711.
  5. Gao, Y. et al. (2018). Effects of farnesoid-X-receptor SUMOylation mutation on myocardial ischemia/reperfusion injury in mice. Exp Cell Res. 371(2):301-310. doi: 10.1016/j.yexcr.2018.07.004.
  6. Wu, B. et al. (2018). Glutaminase 1 regulates the release of extracellular vesicles during neuroinflammation through key metabolic intermediate alpha-ketoglutarate. J Neuroinflammation. 15(1):79. doi: 10.1186/s12974-018-1120-x.
  7. Ansari, S. A. et al. (2016). The role of putative phosphatidylserine-interactive residues of tissue factor on its coagulant activity at the cell surface. PLoS One. doi:10.1371/journal.pone.0158377.
  8. Wang, X. & Astrof, S. (2016). Neural crest cell-autonomous roles of fibronectin in cardiovascular development. Development. 143:88-100.
  9. Bae, E. J. et al. (2015). Cell models to study cell-to-cell transmission of α-synuclein. Methods Mol Biol. 1345:291-298.
  10. Suchanek, A. L. & Salati, L. M. (2015). Construction and evaluation of an adenoviral vector for the liver-specific expression of the serine/arginine-rich splicing factor, SRSF3Plasmid.  doi:10.1016/j.plasmid.2015.07.004.
  11. Wang, S. et al. (2015). Glycoprotein from street rabies virus BD06 induces early and robust immune responses when expressed from a non-replicative adenovirus recombinant. Arch Virol. doi:10.1007/s00705-015-2512-1.
  12. Li, M. et al. (2014). Bisphenol AF-induced endogenous transcription is mediated by ERα and ERK1/2 activation in human breast cancer cells. PLoS One. 9:e94725.
  13. Kim, S. C. et al.  (2014). All‐trans‐retinoic acid ameliorates hepatic steatosis in mice by a novel transcriptional cascade. Hepatology. 59:1750-1760.
  14. Zheng, H. et al. (2014). Inhibition of Endometrial Cancer by n-3 Polyunsaturated Fatty Acids in Preclinical Models. Cancer Prev Res (Phila). 7:824-834.
  15. Logan, S. et al. (2014). Endoplasmic reticulum microenvironment and conserved histidines govern ELOVL4 fatty acid elongase activity. J. Lipid Res. 55:698-708.
  16. Liu, Q. et al. (2013). Evaluation of Rabies Biologics against Irkut Virus Isolated in China. J. Clin. Microbiol. 51:3499-3504.
  17. Logan, S. et al. (2013). Deciphering Mutant ELOVL4 Activity in Autosomal-Dominant Stargardt Macular Dystrophy. PNAS. 110:5446-5451.