Evidence map›Paper›PMID 30469331›Full record

ArticleMolecules (Basel, Switzerland)2018

Selective Inhibition of Human AKR1B10 by

Jan Moritz Seliger, Serhat Sezai Cicek, Lydia T Witt, Hans-Jörg Martin, Edmund Maser, Jan Hintzpeter

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2018. 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
2.3field-weighted citation impact, top 13% 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, 17 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Jan Moritz SeligerInstitute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Brunswikerstr. 10, D-24105 Kiel, Germany. seliger@toxi.uni-kiel.de.ORCID 0000-0003-1337-2850
Serhat Sezai CicekDepartment of Pharmaceutical Biology, Faculty of Mathematics and Natural Sciences, Christian-Albrechts-Universität zu Kiel, Gutenbergstraße 76, D-24118 Kiel, Germany. scicek@pharmazie.uni-kiel.de.ORCID 0000-0002-3038-8523
Lydia T WittDepartment of Pharmaceutical Chemistry, Faculty of Mathematics and Natural Sciences, Christian-Albrechts-Universität zu Kiel, Gutenbergstraße 76, D-24118 Kiel, Germany. lwitt@pharmazie.uni-kiel.de.
Hans-Jörg MartinInstitute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Brunswikerstr. 10, D-24105 Kiel, Germany. martin@toxi.uni-kiel.de.
Edmund MaserInstitute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Brunswikerstr. 10, D-24105 Kiel, Germany. maser@toxi.uni-kiel.de.
Jan HintzpeterInstitute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Brunswikerstr. 10, D-24105 Kiel, Germany. hintzpeter@toxi.uni-kiel.de.
Christian-Albrechts-Universität zu Kiel · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hop-derived compounds have been subjected to numerous biomedical studies investigating their impact on a wide range of pathologies. Isomerised bitter acids (isoadhumulone, isocohumulone and isohumulone) from hops, used in the brewing process of beer, are known to inhibit members of the aldo-keto-reductase superfamily. Aldo-keto-reductase 1B10 (AKR1B10) is upregulated in various types of cancer and has been reported to promote carcinogenesis. Inhibition of AKR1B10 appears to be an attractive means to specifically treat RAS-dependent malignancies. However, the closely related reductases AKR1A1 and AKR1B1, which fulfil important roles in the detoxification of endogenous and xenobiotic carbonyl compounds oftentimes crossreact with inhibitors designed to target AKR1B10. Accordingly, there is an ongoing search for selective AKR1B10 inhibitors that do not interact with endogeneous AKR1A1 and AKR1B1-driven detoxification systems. In this study, unisomerised α-acids (adhumulone, cohumulone and

Indexed as

Aldehyde ReductaseAldo-Keto ReductasesCyclohexanonesCyclohexenesDrug Evaluation, PreclinicalDrug Screening Assays, AntitumorFarnesolGene Expression Regulation, EnzymologicHumansHumulusTerpenesadhumuloneAKR1A1 protein, humanAKR1B10 protein, humanAKR1B1 protein, humanAldehyde ReductaseAldo-Keto ReductasescohumuloneCyclohexanonesCyclohexenesfarnesalFarnesolhumulonTerpenesaldo-keto reductasesalpha-acidscancerfarnesal reductionhopshumulonehumulus lupulusselective inhibitiontight-binding inhibition

Identifiers

PMID30469331
PMCPMC6278539
OpenAlexW2900927838

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.