Evidence map›Paper›PMID 22949619›Full record

ArticleDevelopment (Cambridge, England)2012

An inwardly rectifying K+ channel is required for patterning.

Giri Raj Dahal, Joel Rawson, Brandon Gassaway, Benjamin Kwok, Ying Tong, Louis J Ptácek, Emily Bates

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

77 citing papers in PubMed, 134 citations in OpenAlex.

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  17. Mechanisms Underlying Influence of Bioelectricity in Development.Frontiers in cell and developmental biology · 2022
    Review
  18. Ion Channels and Transporters in Muscle Cell Differentiation.International journal of molecular sciences · 2021
    Review
  19. Role of KInternational journal of molecular sciences · 2021
    Review
  20. Review

17 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Giri Raj DahalDepartment of Chemistry and Biochemistry, Brigham Young University, Provo, UT 84602, USA.
Joel Rawson
Brandon Gassaway
Benjamin Kwok
Ying Tong
Louis J Ptácek
Emily Bates
Brigham Young University · USThe University of Texas Health Science Center at San Antonio · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Mutations that disrupt function of the human inwardly rectifying potassium channel KIR2.1 are associated with the craniofacial and digital defects of Andersen-Tawil Syndrome, but the contribution of Kir channels to development is undefined. Deletion of mouse Kir2.1 also causes cleft palate and digital defects. These defects are strikingly similar to phenotypes that result from disrupted TGFβ/BMP signaling. We use Drosophila melanogaster to show that a Kir2.1 homolog, Irk2, affects development by disrupting BMP signaling. Phenotypes of irk2 deficient lines, a mutant irk2 allele, irk2 siRNA and expression of a dominant-negative Irk2 subunit (Irk2DN) all demonstrate that Irk2 function is necessary for development of the adult wing. Compromised Irk2 function causes wing-patterning defects similar to those found when signaling through a Drosophila BMP homolog, Decapentaplegic (Dpp), is disrupted. To determine whether Irk2 plays a role in the Dpp pathway, we generated flies in which both Irk2 and Dpp functions are reduced. Irk2DN phenotypes are enhanced by decreased Dpp signaling. In wild-type flies, Dpp signaling can be detected in stripes along the anterior/posterior boundary of the larval imaginal wing disc. Reducing function of Irk2 with siRNA, an irk2 deletion, or expression of Irk2DN reduces the Dpp signal in the wing disc. As Irk channels contribute to Dpp signaling in flies, a similar role for Kir2.1 in BMP signaling may explain the morphological defects of Andersen-Tawil Syndrome and the Kir2.1 knockout mouse.

Indexed as

AnimalsAnimals, Genetically ModifiedBody PatterningDrosophilaDrosophila ProteinsEmbryo, MammalianEmbryo, NonmammalianGene Expression Regulation, DevelopmentalMiceMice, KnockoutPhenotypePotassium Channels, Inwardly RectifyingRNA, Small InterferingSignal TransductionWings, Animaldpp protein, DrosophilaDrosophila ProteinsKir2.1 channelPotassium Channels, Inwardly RectifyingRNA, Small Interfering

Identifiers

PMID22949619
PMCPMC3436115
OpenAlexW2051117666

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.