scholarly journals A cell engineering strategy to enhance supercoiled plasmid DNA production for gene therapy

2016 ◽  
Vol 113 (9) ◽  
pp. 2064-2071 ◽  
Author(s):  
Sally Hassan ◽  
Eli Keshavarz-Moore ◽  
John Ward



2011 ◽  
Vol 156 (2) ◽  
pp. 212-222 ◽  
Author(s):  
Vítor M. Gaspar ◽  
Ilídio J. Correia ◽  
Ângela Sousa ◽  
Filomena Silva ◽  
Catarina M. Paquete ◽  
...  


Cell Reports ◽  
2014 ◽  
Vol 8 (6) ◽  
pp. 1677-1685 ◽  
Author(s):  
Elisa Oricchio ◽  
Eirini P. Papapetrou ◽  
Fabien Lafaille ◽  
Yosif M. Ganat ◽  
Sonja Kriks ◽  
...  


Author(s):  
Thomas P. Richardson ◽  
William L. Murphy ◽  
David J. Mooney


Nanoscale ◽  
2021 ◽  
Author(s):  
Zhe Sun ◽  
Jinhai Huang ◽  
Linjia Su ◽  
Jing Li ◽  
Fangzheng Qi ◽  
...  

Using cell-penetrating peptides (CPPs), typically HIV-Tat, to deliver the therapeutic gene for cancer treatment has being hampered by low efficient delivery and complicated uptake route of plasmid DNA (pDNA). On...





FEBS Letters ◽  
1983 ◽  
Vol 153 (1) ◽  
pp. 60-64 ◽  
Author(s):  
Ujjala DasGupta ◽  
Sudhamoy Ghosh


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tugba Mehmetoglu-Gurbuz ◽  
Rose Yeh ◽  
Himanshu Garg ◽  
Anjali Joshi

Abstract Background Gene therapy approaches using hematopoietic stem cells to generate an HIV resistant immune system have been shown to be successful. The deletion of HIV co-receptor CCR5 remains a viable strategy although co-receptor switching to CXCR4 remains a major pitfall. To overcome this, we designed a dual gene therapy strategy that incorporates a conditional suicide gene and CCR5 knockout (KO) to overcome the limitations of CCR5 KO alone. Methods A two-vector system was designed that included an integrating lentiviral vector that expresses a HIV Tat dependent Thymidine Kinase mutant SR39 (TK-SR39) and GFP reporter gene. The second non-integrating lentiviral (NIL) vector expresses a CCR5gRNA-CRISPR/Cas9 cassette and HIV Tat protein. Results Transduction of cells sequentially with the integrating followed by the NIL vector allows for insertion of the conditional suicide gene, KO of CCR5 and transient expression of GFP to enrich the modified cells. We used this strategy to modify TZM cells and generate a cell line that was resistant to CCR5 tropic viruses while permitting infection of CXCR4 tropic viruses which could be controlled via treatment with Ganciclovir. Conclusions Our study demonstrates proof of principle that a combination gene therapy for HIV is a viable strategy and can overcome the limitation of editing CCR5 gene alone.



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