Evidence map›Paper›PMID 26428001›Full record

ArticleBiochemical pharmacology2015

Modulation of ALDH5A1 and SLC22A7 by microRNA hsa-miR-29a-3p in human liver cells.

Dianke Yu, William H Tolleson, Bridgett Knox, Yaqiong Jin, Lei Guo, Yongli Guo, Susan A Kadlubar, Baitang Ning

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  4. miR-15a-3p Protects Against Isoniazid-Induced Liver InjuryFrontiers in molecular biosciences · 2021
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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

8 authors at 4 institutions in 2 countries.

Dianke YuNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
William H TollesonNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Bridgett KnoxNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Yaqiong JinBeijing Children's Hospital, Capital Medical University, Beijing 100045, China.
Lei GuoNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Yongli GuoBeijing Children's Hospital, Capital Medical University, Beijing 100045, China.
Susan A KadlubarUniversity of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Baitang NingNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA. Electronic address: baitang.ning@fda.hhs.gov.
National Center for Toxicological Research · USCapital Medical University · CNUnited States Food and Drug Administration · USUniversity of Arkansas for Medical Sciences · US

Funding

Intramural FDA HHS FD999999
6 · The paper itself

Abstract

Observed variations in drug responses among patients may result from differences in heritable genetic traits or from alterations in the epigenetic regulation of drug metabolizing enzymes and transporters (DMETs). MicroRNAs (miRNAs), a group of small non-coding RNAs, provide an epigenetic mechanism for fine-tuning the expression of targeted DMET genes by regulating the efficiency of protein translation and by decreasing mRNA stability via enhanced degradation. In the current study we systematically screened 374 important genes encoding DMETs for potential response elements to hsa-miR-29a-3p, a highly abundant miRNA in human liver. RNA electrophoresis mobility shift assays displayed direct interactions between hsa-miR-29a-3p and its cognate targets within the mRNA transcripts for the ABCC6, SLC22A7 and ALDH5A1 genes. The expression of luciferase reporter genes containing the 3'-UTRs of SLC22A7 or ALDH5A1 and the expression of endogenous SLC22A7 and ALDH5A1 were each suppressed by transfection with hsa-miR-29a-3p mimics. Importantly, chemically-induced up-regulation of hsa-miR-29a-3p correlated inversely with the expression of SLC22A7 and ALDH5A1. However, our studies failed to detect suppressive effects of hsa-miR-29a-3p on ABCC6 expression, which might be explained by the notion that the interaction of hsa-miR-29a-3p and ABCC6 mRNA was unable to recruit ribonucleoproteins to form a RNA-induced silencing complex.

Indexed as

HEK293 CellsHepatocytesHep G2 CellsHumansMicroRNAsOrganic Anion Transporters, Sodium-IndependentSuccinate-Semialdehyde DehydrogenaseALDH5A1 protein, humanMicroRNAsMIRN29a microRNA, humanOrganic Anion Transporters, Sodium-IndependentSLC22A7 protein, humanSuccinate-Semialdehyde DehydrogenaseALDH5A1Drug metabolizing enzymes and transportershsa-miR-29a-3pmicroRNAPharmacogenomicsSLC22A7

Identifiers

PMID26428001
PMCPMC5705000
OpenAlexW2176926808

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.