Expression of VL30 Vectors in Human Cells That Are Targets for Gene Therapy

Chakraborty, A. K.; Zink, Mary Ann; Hodgson, Clague P.

doi:10.1006/bbrc.1995.1552

Cited by 13 publications

(7 citation statements)

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“…As shown in Table 1, upon G418 selection, the titers obtained with the MLV-VL30m vectors were of the same order of magnitude as those of the control MLV vector. These data not only confirm the work of Chakraborty et al (20), which suggested that the 5Ј region of VL30m has the ability to drive packaging of a recombinant RNA, but because LacZ is expressed, they also show that VL30m can direct translation of a 3Ј cistron in the context of a monocistronic retroviral vector.…”

Section: Recombinant Mlv-vl30m Vectors Allow Expression Of Lacz In Trsupporting

confidence: 88%

Identification of an Internal Ribosome Entry Segment in the 5′ Region of the Mouse VL30 Retrotransposon and Its Use in the Development of Retroviral Vectors

López-Lastra

Ulrici

Gabus

et al. 1999

J Virol

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Mouse virus-like 30S RNAs (VL30m) constitute a family of retrotransposons, present at 100 to 200 copies, dispersed in the mouse genome. They display little sequence homology to Moloney murine leukemia virus (MoMLV), do not encode virus-like proteins, and have not been implicated in retroviral carcinogenesis. However, VL30 RNAs are efficiently packaged into MLV particles that are propagated in cell culture. In this study, we addressed whether the 5′ region of VL30m could replace the 5′ leader of MoMLV functionally in a recombinant vector construct. Our data confirm that the putative packaging sequence of VL30 is located within the 5′ region (nucleotides 362 to 1149 with respect to the cap structure) and that it can replace the packaging sequence of MoMLV. We also show that VL30m contains an internal ribosome entry segment (IRES) in the 5′ region, as do MoMLV, Friend murine leukemia virus, Harvey murine sarcoma virus, and avian reticuloendotheliosis virus type A. Our data show that both the packaging and IRES functions of the 5′ region of VL30m RNA can be efficiently used to develop retrotransposon-based vectors.

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Section: Recombinant Mlv-vl30m Vectors Allow Expression Of Lacz In Trsupporting

confidence: 88%

Identification of an Internal Ribosome Entry Segment in the 5′ Region of the Mouse VL30 Retrotransposon and Its Use in the Development of Retroviral Vectors

López-Lastra

Ulrici

Gabus

et al. 1999

J Virol

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“…Annual CRISPR 2017 conference, held at Montana State University, we are the first to hear about successes of starter companies like Locus Bioscience and Eligo Bioscience using CRISPR-Cas technology to kill the superbug targeting mdr genes [82]. In this method, a short RNA and a short oligonucleotide match could be engineered to CRISPR-complex to cleave mRNA of superbug by endonuclease activity of enzyme.…”

Section: Crispr-cas Technologymentioning

confidence: 99%

Heterogeneous Phyto-Antibiotics and Other Future Therapeutics Against Multi-Drug Resistant Bacteria

Chakraborty¹

2019

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Phage therapy, enzybiotics, gene medicine and nanodrug-carriers are most vital components of modern research against multidrug-resistant bacteria. Genome evolution occurs due to environmental toxicities of various types where soil bacteria are in symbiosis with plant world who secret anti-metabolites against soil bacteria. Gut microbiome secrete vitamins required for our body where as intestinal cells synthesis interleukins and cytokines for symbiotic control of intestinal bacteria. Before the discovery of antibiotic in 1928, peoples trusted plant derived remedies against variety of illness described in Indian Sanskrit books like Charaka Samhita, Sasruta Samhita and Atharva Veda. AMR disease occurred due to repeated but uncontrolled use of antibiotics affecting gut microbiome who acquired many mdr genes in plasmids. We estimated that 40% of all river and sea water borne bacteria were ampicillin and to lesser extent tetracycline, azithromycin, ciprofloxacin and streptomycin resistant. Where as <1% were multidrug-resistant and ~0.002% Enterobacteriaceae were meropenem, linezolid or amikacin resistant. MDR genes like amp, neo, tet, aac, cat, aph, aad, arr3, sul1, dhfr, inh, acrAB, mexAB, macAB and mtrCD were amplified with millions mutated isomers increasing all drugs MIC. We studied Indian medicinal plants and spices to get valuable cheap drugs where modified agriculture and/or tissue culture increased the drug concentration. We showed that MDR bacteria were sensitive to organic extract of Suregada multiflora roots, Cassia fistula bark, Jatropha gossypifolia roots as well as Indian spices Labanga and Derchini (MDR-Cure). TLC and HPLC purification as well as UV-VIS, MASS, NMR, FT-IR and XRD-Powder gave many distinct signatures of pure chemicals that also inhibited multidrug-resistant bacteria. Biological targets of 12 chemicals are under investigation targeting DNA Topoisomerase I, DNA Polymerase and RNA Polymerase of Escherichia coli. Indian Government has started Herbal Mission, Ganga Mission and various Plantation Programmes to curve MDR pathogenesis.

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“…We must consider security, absence of pathogens, traceability of the parental cell, and a low rate of homologous recombination. Furthermore, the fact that endogenous retroviruses can compete for packaging imposes careful selection of the candidate producing cells 76–78. NIH 3T3 were the first cells and, along with the gibbon‐derived PG13, are the only ones that have received a licence to produce virus for clinical trial 79.…”

Section: Main Course: Retrovirus and Cellmentioning

confidence: 99%