Evidence map›Paper›PMID 28818080›Full record

ArticleJournal of biomedical science2017

Standardized, systemic phenotypic analysis reveals kidney dysfunction as main alteration of Kctd1

Sudhir Kumar, Birgit Rathkolb, Sibylle Sabrautzki, Stefan Krebs, Elisabeth Kemter, Lore Becker, Johannes Beckers, Raffi Bekeredjian, Robert Brommage, Julia Calzada-Wack and 13 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  5. Review
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

23 authors at 6 institutions in 2 countries.

Sudhir KumarChair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, 81377, Munich, Germany.
Birgit RathkolbChair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, 81377, Munich, Germany.
Sibylle SabrautzkiGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Stefan KrebsChair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, 81377, Munich, Germany.
Elisabeth KemterChair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, 81377, Munich, Germany.
Lore BeckerGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Johannes BeckersGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Raffi BekeredjianDepartment of Medicine III, Division of Cardiology, University of Heidelberg, 69120, Heidelberg, Germany.
Robert BrommageGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Julia Calzada-WackGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Lillian GarrettGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Sabine M HölterGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Marion HorschGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Martin KlingensporMolecular Nutritional Medicine, Else Kröner-Fresenius Center, TU Munich, 85350, Freising-Weihenstephan, Germany.
Thomas KlopstockDepartment of Neurology, Friedrich-Baur-Institute, University Hospital Munich, 80336, Munich, Germany.
Kristin MorethGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Frauke NeffInstitute of Pathology, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Jan RozmanGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Helmut FuchsGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Valérie Gailus-DurnerGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Martin Hrabe de AngelisGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Eckhard WolfChair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, 81377, Munich, Germany.
Bernhard AignerChair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, 81377, Munich, Germany. b.aigner@gen.vetmed.uni-muenchen.de.ORCID http://orcid.org/0000-0003-1644-2711
Helmholtz Zentrum München · DELudwig-Maximilians-Universität München · DEFresenius (Germany) · DEGene Therapy Laboratory · FRGerman Center for Neurodegenerative Diseases · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreased levels of blood plasma urea were used as phenotypic parameter for establishing novel mouse models for kidney diseases on the genetic background of C3H inbred mice in the phenotype-driven Munich ENU mouse mutagenesis project. The phenotypically dominant mutant line HST014 was established and further analyzed.

methodsAnalysis of the causative mutation as well as the standardized, systemic phenotypic analysis of the mutant line was carried out.

resultsThe causative mutation was detected in the potassium channel tetramerization domain containing 1 (Kctd1) gene which leads to the amino acid exchange Kctd1

conclusionsIn summary, the main alteration of the Kctd1

Indexed as

Disease Models, AnimalMiceMutationAnimalsCo-Repressor ProteinsFemaleKidneyKidney DiseasesMaleMice, Inbred C3HPhenotypeCo-Repressor ProteinsKctd1 protein, mouseAnimal modelKctd1SEN syndromeSystematic phenotype analysis

Identifiers

PMID28818080
PMCPMC5559776
OpenAlexW2748943230

What OpenQuestion holds

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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.