Evidence map›Paper›PMID 26442203›Full record

ArticleFEBS open bio2015

The AQP2 mutation V71M causes nephrogenic diabetes insipidus in humans but does not impair the function of a bacterial homolog.

Noreen Klein, Nadine Kümmerer, Dominika Hobernik, Dirk Schneider

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS open bio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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

4 authors at 1 institution in 1 country.

Noreen KleinInstitut für Pharmazie und Biochemie, Johannes Gutenberg-Universität Mainz, 55128 Mainz, Germany.
Nadine KümmererInstitut für Pharmazie und Biochemie, Johannes Gutenberg-Universität Mainz, 55128 Mainz, Germany.
Dominika HobernikInstitut für Pharmazie und Biochemie, Johannes Gutenberg-Universität Mainz, 55128 Mainz, Germany.
Dirk SchneiderInstitut für Pharmazie und Biochemie, Johannes Gutenberg-Universität Mainz, 55128 Mainz, Germany.
Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several point mutations have been identified in human aquaporins, but their effects on the function of the respective aquaporins are mostly enigmatic. We analyzed the impact of the aquaporin 2 mutation V71M, which causes nephrogenic diabetes insipidus in humans, on aquaporin structure and activity, using the bacterial aquaglyceroporin GlpF as a model. Importantly, the sequence and structure around the V71M mutation is highly conserved between aquaporin 2 and GlpF. The V71M mutation neither impairs substrate flux nor oligomerization of the aquaglyceroporin. Therefore, the human aquaporin 2 mutant V71M is most likely active, but cellular trafficking is probably impaired.

Indexed as

ActivityAQP, aquaporinAQP ER, endoplasmic reticulumAquaporinAVP, arginine vasopressinAVPR2, V2 receptorGlpFGlpF, glycerol facilitatorGpA, glycophorin AHM, half-membrane-spanningNDI, nephrogenic diabetes insipidusNephrogenic diabetes insipidusProtein oligomerizationTM, transmembranewt, wild-type

Identifiers

PMID26442203
PMCPMC4552806
OpenAlexW1458736145

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.