Evidence map›Paper›PMID 25940378›Full record

ArticleBMC neuroscience2015

Increase in the titer of lentiviral vectors expressing potassium channels by current blockade during viral vector production.

Masayoshi Okada, Naaz Andharia, Hiroko Matsuda

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Hypothalamic Ion Channels in Hypertension.Current hypertension reports · 2018
    Review
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Masayoshi OkadaDepartment of Physiology, Kansai Medical University, 2-5-1 Shin-machi, Hirakata, Osaka, 573-1010, Japan. mokada-tky@umin.ac.jp.
Naaz AndhariaDepartment of Physiology, Kansai Medical University, 2-5-1 Shin-machi, Hirakata, Osaka, 573-1010, Japan. naaz.andharia@yahoo.com.
Hiroko MatsudaDepartment of Physiology, Kansai Medical University, 2-5-1 Shin-machi, Hirakata, Osaka, 573-1010, Japan. matsudah@hirakata.kmu.ac.jp.
Kansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh titers of lentiviral vectors are required for the efficient transduction of a gene of interest. During preparation of lentiviral the vectors, the protein of interest is inevitably expressed in the viral vector-producing cells. This expression may affect the production of the lentiviral vector.

methodsWe prepared lentiviral vectors expressing inwardly rectifying potassium channel (Lv-Kir2.1), its dominant-negative form (Lv-Kir-DN), and other K(+) channels, using the ubiquitously active β-actin and neuron-specific synapsin I promoters.

resultsThe titer of Lv-Kir-DN was higher than that of Lv-Kir2.1, suggesting a negative effect of induced K(+) currents on viral titer. We then blocked Kir2.1 currents with the selective blocker Ba(2+) during Lv-Kir2.1 production, and obtained about a 5-fold increase in the titer. Higher extracellular K(+) concentrations increased the titer of Lv-Kir2.1 about 9-fold. With a synapsin I promoter Ba(2+) increased the titer because of the moderate expression of Kir2.1 channel. Channel blockade also increased the titers of the lentivirus expressing Kv1.4 and TREK channels, but not HERG. The increase in titer correlated with the K(+) currents generated by the channels expressed.

conclusionIn the production of lentivirus expressing K(+) channels, titers are increased by blocking K(+) currents in the virus-producing cells. This identifies a crucial issue in the production of viruses expressing membrane channels, and should facilitate basic and gene therapeutic research on channelopathies.

Indexed as

Genetic VectorsAnimalsBariumCations, DivalentERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsExtracellular SpaceHEK293 CellsHippocampusHumansKv1.4 Potassium ChannelLentivirusMembrane PotentialsNeuronsPotassiumPotassium Channel BlockersBariumCations, DivalentERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsKCNH2 protein, humanKir2.1 channelKv1.4 Potassium ChannelPotassiumPotassium Channel Blockerspotassium channel protein TREK-1Potassium Channels, Inwardly RectifyingPotassium Channels, Tandem Pore DomainSynapsins

Identifiers

PMID25940378
PMCPMC4425897
OpenAlexW1919132789

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.