ArticleNucleic acid therapeutics2014
Gamma-retroviral vector design for the co-expression of artificial microRNAs and therapeutic proteins.
Article in Nucleic acid therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- CAR signaling instructs divergent metabolic reprogramming and functional fates in αβ and γδ T cells.Cellular & molecular immunology · 2026Article
- MicroRNAs in Breast Cancer: Biological Functions and Technologies for Experimental and Therapeutic Applications.Cancers · 2026Review
- IL-12-secreting CAR-T cells reprogram the tumor microenvironment and improve efficacy against heterogeneous models of glioblastoma.Journal for immunotherapy of cancer · 2026Article
- Gamma-retrovirus design for efficacious microRNA-mediated gene knock-down and protein co-expression without compromising titers.NAR molecular medicine · 2025Article
- Article
- Methods of miRNA delivery and possibilities of their application in neuro-oncology.Non-coding RNA research · 2023Review
- γδ-Enriched CAR-T cell therapy for bone metastatic castrate-resistant prostate cancer.Science advances · 2023Article
- Use of phage display biopanning as a tool to design CAR-T cells against glioma stem cells.Frontiers in oncology · 2023Article
- An immunoproteomic approach to characterize the CAR interactome and signalosome.Science signaling · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To generate γ-retroviral vectors for stable conjoint expression of artificial microRNAs (amiR) and therapeutic genes in primary human lymphocytes, and to identify the design parameters that are key for successful vector generation. Gamma-retroviral vectors were designed to co-express both amiRs and a linked reporter gene, truncated CD34 (tCD34). Artificial miRs based on microRNAs miR-16, miR-142, miR-146b, miR-150, miR155, and miR-223 were inserted into sites within the intron of the vector and tested for tCD34 expression by flow cytometry (FACS). Different constructs were assembled with amiRs targeted to knockdown expression of suppressor of cytokine signaling 1 (SOCS1) or programmed cell death 1 (PDCD1, PD-1). Three of the six amiRs maintained tCD34 expression. Expansion of primary human T cells transduced with these amiR vectors, as well as transgene expression, were equivalent to control engineered T cells over a 40-day period. Knockdown of SOCS1 RNA and PD-1 expression by FACS was shown to vary between constructs, dependent on either the specific short interfering RNA sequence used in the amiR, or the microRNA backbone and location in the vector intron. Gamma-retroviral vectors that both efficiently knockdown endogenous gene expression and maintain linked transgene production can be produced, but empirical vector evaluations were best suited for optimal construct analysis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.