ArticleDevelopmental cell2017
A Wnt5 Activity Asymmetry and Intercellular Signaling via PCP Proteins Polarize Node Cells for Left-Right Symmetry Breaking.
Open access · bronzeAbstract read
In one paragraph
Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
9.9field-weighted citation impact, top 1% of its field
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.
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.
Who cites it
70 citing papers in PubMed, 113 citations in OpenAlex.
- Epithelial-mesenchymal Wnt crosstalk directs planar cell polarity in the developing cochlea.Nature communications · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Article
- Epithelial-Mesenchymal Wnt Crosstalk Directs Planar Cell Polarity in the Developing Cochlea.bioRxiv : the preprint server for biology · 2026Article
- Planar cell polarity emerges through polarized accumulation of Wnt11.Science advances · 2026Article
- Differential functions of multiple Wnts and receptors in cell polarity regulation inbioRxiv : the preprint server for biology · 2025Article
- A conserved domain of Cfap298 governs left-right symmetry breaking in vertebrates.Journal of cell science · 2025Article
- Planar cell polarity coordination in a cnidarian embryo provides clues to animal body axis evolution.eLife · 2025Article
- Notch3 is an asymmetric gene and a modifier of heart looping defects in Nodal mouse mutants.PLoS biology · 2025Article
- Bilateral cellular flows display asymmetry prior to left-right organizer formation in amniote gastrulation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Decoding Epilepsy: Prickle2 and Multifaceted Molecular Pathway Connections.Current pharmaceutical design · 2025Review
- Bilateral cellular flows display asymmetry prior to left-right organizer formation in amniote gastrulation.bioRxiv : the preprint server for biology · 2024Article
- Breaking Left-Right Symmetry by the Interplay of Planar Cell Polarity, Calcium Signaling and Cilia.Cells · 2024Review
- Clinical Potential of Misshapen/NIKs-Related Kinase (MINK) 1-A Many-Sided Element of Cell Physiology and Pathology.Current issues in molecular biology · 2024Review
- Review
- Canonical and Non-Canonical Wnt Signaling Generates Molecular and Cellular Asymmetries to Establish Embryonic Axes.Journal of developmental biology · 2024Review
- Myosin1G promotes Nodal signaling to control zebrafish left-right asymmetry.Nature communications · 2024Article
- A fibronectin gradient remodels mixed-phase mesoderm.Science advances · 2024Article
- Wnt5 controls splenic myelopoiesis and neutrophil functional ambivalency during DSS-induced colitis.Cell reports · 2024Article
- Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
19 authors at 8 institutions in 2 countries.
Katsura MinegishiDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan; Laboratory for Organismal Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan. Electronic address: katsura.minegishi@riken.jp.
Masakazu HashimotoDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan.
Rieko AjimaDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan; Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute-Frederick, NIH, Frederick, MD 21702, USA.
Katsuyoshi TakaokaDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan.
Kyosuke ShinoharaDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan.
Yayoi IkawaDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan; Laboratory for Organismal Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Hiromi NishimuraDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan; Laboratory for Organismal Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Andrew P McMahonDepartment of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA.
Karl WillertDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA 92093, USA.
Yasushi OkadaLaboratory for Cell Polarity Regulation, RIKEN Quantitative Biology Center, 6-2-3 Furuedai, Suita, Osaka 565-0874, Japan.
Hiroshi SasakiLaboratory for Embryogenesis, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan.
Dongbo ShiDivision of Embryology, National Institute for Basic Biology, 5-1 Higashiyama, Myodaiji, Okazaki, Aichi 444-8787, Japan.
Toshihiko FujimoriDivision of Embryology, National Institute for Basic Biology, 5-1 Higashiyama, Myodaiji, Okazaki, Aichi 444-8787, Japan.
Toshihisa OhtsukaDepartment of Biochemistry, Faculty of Medicine/Graduate School of Medicine, University of Yamanashi, 1110 Shimo-Kato, Chuo, Yamanashi 409-3898, Japan.
Yasunobu IgarashiAdvanced Software Development Department, OLYMPUS Software Technology Corporation, 2-3 Kuboyama-cho, Hachioji-shi, Tokyo 192-8512, Japan.
Terry P YamaguchiCancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute-Frederick, NIH, Frederick, MD 21702, USA.
Akihiko ShimonoVertebrate Body Plan Group, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Hidetaka ShiratoriDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan.
Hiroshi HamadaDevelopmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan; Laboratory for Organismal Patterning, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan. Electronic address: hiroshi.hamada@riken.jp.
Osaka University · JPNational Cancer Institute · USNational Institute for Basic Biology · JPOlympus (Japan) · JPRIKEN Center for Computational Science · JPUniversity of California, San Diego · USUniversity of Southern California · USUniversity of Yamanashi · JP
Funding
The Role of Wnt Genes in Vertebrate Development and CancerZIABC010345 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YAMAGUCHI, TERENCE · 2009 to 2025
$23.3MRegulation of polarity by Sonic hedgehog morphogen signalingR01NS033642 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MCMAHON, ANDREW P. · 1995 to 2016
$5.7MThe Role of Wnt Genes in Vertebrate Gastrointestinal DevZ01BC010345 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YAMAGUCHI, TERENCE · 2000 to 2008
$1.2MIntramural NIH HHS Z01 BC010345Intramural NIH HHS ZIA BC010345NINDS NIH HHS R01 NS033642
Abstract
Polarization of node cells along the anterior-posterior axis of mouse embryos is responsible for left-right symmetry breaking. How node cells become polarized has remained unknown, however. Wnt5a and Wnt5b are expressed posteriorly relative to the node, whereas genes for Sfrp inhibitors of Wnt signaling are expressed anteriorly. Here we show that polarization of node cells is impaired in Wnt5a
Indexed as
Body PatterningCell PolaritySignal TransductionAdaptor Proteins, Signal TransducingAnimalsCell CommunicationFrizzled-Related ProteinsIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMembrane ProteinsMiceMice, Mutant StrainsModels, BiologicalProteinsWnt-5a ProteinWnt ProteinsAdaptor Proteins, Signal TransducingFrizzled-Related ProteinsIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMembrane ProteinsPrickle1 protein, mousePrickle2 protein, mouseProteinsWnt-5a ProteinWnt5a protein, mouseWnt5b protein, mouseWnt Proteinsbasal bodybreaking of left-right symmetryciliaplanar cell polaritySfrpWnt
Identifiers
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.