Evidence map›Paper›PMID 26455426›Full record

ArticleScientific reports2015

Functional identification of SLC43A3 as an equilibrative nucleobase transporter involved in purine salvage in mammals.

Junji Furukawa, Katsuhisa Inoue, Junya Maeda, Tomoya Yasujima, Kinya Ohta, Yoshikatsu Kanai, Tappei Takada, Hirotaka Matsuo, Hiroaki Yuasa

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Inborn Errors of Nucleoside Transporter (NT)-Encoding Genes (International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Junji FurukawaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Katsuhisa InoueDepartment of Biopharmaceutics, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Junya MaedaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Tomoya YasujimaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Kinya OhtaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Yoshikatsu KanaiDivision of Bio-system Pharmacology, Department of Pharmacology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tappei TakadaDepartment of Pharmacy, The University of Tokyo Hospital, Tokyo, Japan.
Hirotaka MatsuoDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, Saitama, Japan.
Hiroaki YuasaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Nagoya City University · JPNational Defense Medical College · JPOsaka University · JPTokyo University of Pharmacy and Life Sciences · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purine salvage pathway plays a major role in the nucleotide production, relying on the supply of nucleobases and nucleosides from extracellular sources. Although specific transporters have been suggested to be involved in facilitating their transport across the plasma membrane in mammals, those which are specifically responsible for utilization of extracellular nucleobases remain unknown. Here we present the molecular and functional characterization of SLC43A3, an orphan transporter belonging to an amino acid transporter family, as a purine-selective nucleobase transporter. SLC43A3 was highly expressed in the liver, where it was localized to the sinusoidal membrane of hepatocytes, and the lung. In addition, SLC43A3 expressed in MDCKII cells mediated the uptake of purine nucleobases such as adenine, guanine, and hypoxanthine without requiring typical driving ions such as Na(+) and H(+), but it did not mediate the uptake of nucleosides. When SLC43A3 was expressed in APRT/HPRT1-deficient A9 cells, adenine uptake was found to be low. However, it was markedly enhanced by the introduction of SLC43A3 with APRT. In HeLa cells, knock-down of SLC43A3 markedly decreased adenine uptake. These data suggest that SLC43A3 is a facilitative and purine-selective nucleobase transporter that mediates the cellular uptake of extracellular purine nucleobases in cooperation with salvage enzymes.

Indexed as

AdenineAdenine PhosphoribosyltransferaseAdenosineAmino Acid Transport SystemsAnimalsBiological TransportDogsEquilibrative Nucleoside Transporter 1HEK293 CellsHeLa CellsHepatocytesHumansHypoxanthineLiverLungMadin Darby Canine Kidney CellsAdenineAdenine PhosphoribosyltransferaseAdenosineAmino Acid Transport SystemsEquilibrative Nucleoside Transporter 1HypoxanthineProtein IsoformsPurinesRNA, Small InterferingSLC43A3 protein, humanThymidineUridine

Identifiers

PMID26455426
PMCPMC4796657
OpenAlexW2285208220

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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.