ArticleDevelopmental biology2010
In vivo analysis in Drosophila reveals differential requirements of contact residues in Axin for interactions with GSK3beta or beta-catenin.
Article in Developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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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.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Uncovering phenotypic expansion in AXIN2-related disorders through precision animal modeling.Genetics in medicine : official journal of the American College of Medical Genetics · 2026Article
- Reconstructing the evolutionary origin of β-catenin recognition in the Wnt destruction complex.Molecular biology and evolution · 2026Article
- An early global role for Axin is required for correct patterning of the anterior-posterior axis in the sea urchin embryo.Development (Cambridge, England) · 2021Article
- Divergent Axin and GSK-3 paralogs in the beta-catenin destruction complexes of tapeworms.Development genes and evolution · 2019Article
- Wnt/Beta-Catenin Signaling Regulation and a Role for Biomolecular Condensates.Developmental cell · 2019Review
- Identification of Proteins Required for Precise Positioning of Apc2 in Dendrites.G3 (Bethesda, Md.) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Proper regulation of the Wingless/Wnt signaling pathway is essential for normal development. The scaffolding protein Axin plays a key role in this process through interactions with Drosophila Shaggy and Armadillo. In the current studies, we used a yeast two-hybrid assay to identify ten amino acids in Axin that are critical for in vitro interaction with Shaggy and two for interaction with Armadillo. We then generated five Axin variants in which individual putative contact amino acids were mutated and compared their activity, as assayed by rescue of axin null mutant flies, to that of Axin lacking the entire Shaggy (AxinDeltaSgg) or Armadillo (AxinDeltaArm) binding domain. Although we expected these mutants to function identically to Axin in which the entire binding domain was deleted, we instead observed a spectrum of phenotypic rescue. Specifically, two point mutants within the Shaggy binding domain showed loss of activity similar to that of AxinDeltaSgg and dominantly interfered with complex function, whereas a third mutant allele, AxinK446E, retained most function. Two Axin point mutants within the Armadillo binding domain were weak alleles and retained most function. These findings demonstrate the importance of in vivo verification of the role of specific amino acids within a protein.
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Registered trials
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.