Evidence map›Paper›PMID 20300656›Full record

ArticlePLoS genetics2010

Arginylation-dependent neural crest cell migration is essential for mouse development.

Satoshi Kurosaka, N Adrian Leu, Fangliang Zhang, Ralph Bunte, Sougata Saha, Junling Wang, Caiying Guo, Wei He, Anna Kashina

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.8field-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

48 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Methods to Study Arginylation of Tubulin.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  3. Article
  4. Method Overview for Discovering ATE1 Substrates and their Arginylation Sites.Chembiochem : a European journal of chemical biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Protein Arginylation: Milestones of Discovery.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Posttranslational modifications of the cytoskeleton.Cytoskeleton (Hoboken, N.J.) · 2021
    Review
  14. Article
  15. Arginylation Regulates G-protein Signaling in the Retina.Frontiers in cell and developmental biology · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Satoshi KurosakaDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
N Adrian Leu
Fangliang Zhang
Ralph Bunte
Sougata Saha
Junling Wang
Caiying Guo
Wei He
Anna Kashina
University of Pennsylvania · USJanelia Research Campus · USUConn Health · US

Funding

Role of Protein Arginylation in Cardiovascular DevelopmentR01HL084419 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KASHINA, ANNA S · 2007 to 2011
$2.2M
NHLBI NIH HHS 5R01HL084419NHLBI NIH HHS R01 HL084419
6 · The paper itself

Abstract

Coordinated cell migration during development is crucial for morphogenesis and largely relies on cells of the neural crest lineage that migrate over long distances to give rise to organs and tissues throughout the body. Recent studies of protein arginylation implicated this poorly understood posttranslational modification in the functioning of actin cytoskeleton and in cell migration in culture. Knockout of arginyltransferase (Ate1) in mice leads to embryonic lethality and severe heart defects that are reminiscent of cell migration-dependent phenotypes seen in other mouse models. To test the hypothesis that arginylation regulates cell migration during morphogenesis, we produced Wnt1-Cre Ate1 conditional knockout mice (Wnt1-Ate1), with Ate1 deletion in the neural crest cells driven by Wnt1 promoter. Wnt1-Ate1 mice die at birth and in the first 2-3 weeks after birth with severe breathing problems and with growth and behavioral retardation. Wnt1-Ate1 pups have prominent defects, including short palate and altered opening to the nasopharynx, and cranial defects that likely contribute to the abnormal breathing and early death. Analysis of neural crest cell movement patterns in situ and cell motility in culture shows an overall delay in the migration of Ate1 knockout cells that is likely regulated by intracellular mechanisms rather than extracellular signaling events. Taken together, our data suggest that arginylation plays a general role in the migration of the neural crest cells in development by regulating the molecular machinery that underlies cell migration through tissues and organs during morphogenesis.

Indexed as

Cell MovementGrowth and DevelopmentAminoacyltransferasesAnimalsAnimals, NewbornArginineBone and BonesCell AdhesionCells, CulturedCoculture TechniquesCraniofacial AbnormalitiesGene Knockout TechniquesMesodermMiceMice, KnockoutModels, BiologicalAminoacyltransferasesArgininearginyltransferaseWnt1 ProteinWnt1 protein, mouse

Identifiers

PMID20300656
PMCPMC2837401
OpenAlexW2041063347

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.