Evidence map›Paper›PMID 29571612›Full record

ArticleDevelopmental biology2018

Kir2.1 is important for efficient BMP signaling in mammalian face development.

Matthew T Belus, Madison A Rogers, Alaaeddin Elzubeir, Megan Josey, Steven Rose, Viktoria Andreeva, Pamela C Yelick, Emily A Bates

Abstract read
In one paragraph

Article in Developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

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  19. Evolution of inwardly rectifying potassium channels and their gene expression in zebrafish embryos.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
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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 2 institutions in 1 country.

Matthew T BelusDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, United States.
Madison A RogersDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, United States.
Alaaeddin ElzubeirDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, United States.
Megan JoseyDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, United States.
Steven RoseDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, United States.
Viktoria AndreevaDepartment of Orthodontics, Division of Craniofacial and Molecular Genetics, Tufts University, Boston, MA 02111, United States.
Pamela C YelickDepartment of Orthodontics, Division of Craniofacial and Molecular Genetics, Tufts University, Boston, MA 02111, United States.
Emily A BatesDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045, United States. Electronic address: emily.bates@ucdenver.edu.
University of Colorado Denver · USTufts University · US

Funding

Ion channel mediated control of mophogen signaling for craniofacial development in mammalsR01DE025311 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI BATES, EMILY · 2018 to 2023
$1.8M
Ion channel mediated control of mophogen signaling for craniofacial development in mammalsR56DE025311 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI BATES, EMILY · 2015 to 2015
$386k
NIDCR NIH HHS R01 DE025311NIDCR NIH HHS R56 DE025311
6 · The paper itself

Abstract

Mutations that disrupt the inwardly rectifying potassium channel Kir2.1 lead to Andersen-Tawil syndrome that includes periodic paralysis, cardiac arrhythmia, cognitive deficits, craniofacial dysmorphologies and limb defects. The molecular mechanism that underlies the developmental consequences of inhibition of these channels has remained a mystery. We show that while loss of Kir2.1 function does not affect expression of several early facial patterning genes, the domain in which Pou3f3 is expressed in the maxillary arch is reduced. Pou3f3 is important for development of the jugal and squamosal bones. The reduced expression domain of Pou3f3 is consistent with the reduction in the size of the squamosal and jugal bones in Kcnj2

Indexed as

AnimalsBody PatterningBone Morphogenetic ProteinsCraniofacial AbnormalitiesFaceGene Expression RegulationMiceMice, KnockoutMutationNerve Tissue ProteinsNeural CrestPotassium Channels, Inwardly RectifyingPOU Domain FactorsSignal TransductionSkullTranscription FactorsBone Morphogenetic ProteinsKir2.1 channelNerve Tissue ProteinsPotassium Channels, Inwardly RectifyingPou3f3 protein, mousePOU Domain FactorsTranscription Factors

Identifiers

PMID29571612
PMCPMC6148416
OpenAlexW2791127491

What OpenQuestion holds

Textmetadata
LicenceTDM
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.