ArticleGenes2018
Identification of a WNT5A-Responsive Degradation Domain in the Kinesin Superfamily Protein KIF26B.
Article in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- The C-terminal region of KIF26B is indispensable for nephron progenitor condensation and kidney formation in mice.FEBS open bio · 2026Article
- Local Misalignment Scoring Reveals Spatially Uniform Chondrocyte Disorganization in a Wnt5a-C83S Knock-in Model of Robinow Syndrome.Research square · 2025Article
- Identification of Vesicle-Mediated Transport-Related Genes for Predicting Prognosis, Immunotherapy Response, and Drug Screening in Cervical Cancer.Immunity, inflammation and disease · 2024Article
- The Kinesin GeneInternational journal of molecular sciences · 2022Article
- KIF26B in the Prognosis and Immune Biomarking of Various Cancers: A Pan-Cancer Study.Journal of oncology · 2022Article
- Roles of Wnt Signaling Pathway and ROR2 Receptor in Embryonic Development: An Update Review Article.Epigenetics insights · 2022Article
- ELK1-induced up-regulation of KIF26B promotes cell cycle progression in breast cancer.Medical oncology (Northwood, London, England) · 2021Article
- Review
- Oxidized Low-Density Lipoprotein Induces WNT5A Signaling Activation in THP-1 Derived Macrophages and a Human Aortic Vascular Smooth Muscle Cell Line.Frontiers in cardiovascular medicine · 2020Article
- Noncoding RNAs-based high KIF26B expression correlates with poor prognosis and tumor immune infiltration in colon cancer.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Noncanonical WNT pathways function independently of the β-catenin transcriptional co-activator to regulate diverse morphogenetic and pathogenic processes. Recent studies showed that noncanonical WNTs, such as WNT5A, can signal the degradation of several downstream effectors, thereby modulating these effectors' cellular activities. The protein domain(s) that mediates the WNT5A-dependent degradation response, however, has not been identified. By coupling protein mutagenesis experiments with a flow cytometry-based degradation reporter assay, we have defined a protein domain in the kinesin superfamily protein KIF26B that is essential for WNT5A-dependent degradation. We found that a human disease-causing KIF26B mutation located at a conserved amino acid within this domain compromises the ability of WNT5A to induce KIF26B degradation. Using pharmacological perturbation, we further uncovered a role of glycogen synthase kinase 3 (GSK3) in WNT5A regulation of KIF26B degradation. Lastly, based on the identification of the WNT5A-responsive domain, we developed a new reporter system that allows for efficient profiling of WNT5A-KIF26B signaling activity in both somatic and stem cells. In conclusion, our study identifies a new protein domain that mediates WNT5A-dependent degradation of KIF26B and provides a new tool for functional characterization of noncanonical WNT5A signaling in cells.
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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.