ArticleThe Journal of biological chemistry2013
Functional consequences of Wnt-induced dishevelled 2 phosphorylation in canonical and noncanonical Wnt signaling.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Genetic screening identifies WNT5A/RYK as a determinant of extracellular vesicle fate.Science advances · 2026Article
- A Wnt-induced conformational phospho-switch in DVL3 controls association with Frizzled receptors and Wnt/β-catenin signaling.Science advances · 2026Article
- From Motor Proteins to Oncogenic Factors: The Evolving Role of Kinesin Superfamily Proteins in Breast Cancer Development.Molecular biotechnology · 2026Review
- Coupling mathematical modeling with a novel human intestinal stem cell system to understand feedback regulation during planar cell polarity.bioRxiv : the preprint server for biology · 2025Article
- Evolutionary conservation and cancer implications of the WNT signaling pathway.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Vangl-dependent Wnt/planar cell polarity signaling mediates collective breast carcinoma motility and distant metastasis.Breast cancer research : BCR · 2023Article
- The complex relationship of Wnt-signaling pathways and cilia.Current topics in developmental biology · 2023Article
- DIX domain containing 1 (DIXDC1) modulates VEGFR2 level in vasculatures to regulate embryonic and postnatal retina angiogenesis.BMC biology · 2022Article
- Dvl2 facilitates the coordination of NF-κB and Wnt signaling to promote colitis-associated colorectal progression.Cancer science · 2022Article
- The CK1δ/ϵ-Tip60 Axis Enhances Wnt/β-Catenin SignalingFrontiers in oncology · 2022Article
- Loss of Zic3 impairs planar cell polarity leading to abnormal left-right signaling, heart defects and neural tube defects.Human molecular genetics · 2021Article
- Article
- Regulation of Dishevelled DEP domain swapping by conserved phosphorylation sites.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Activated ALK Cooperates with N-Myc via Wnt/β-Catenin Signaling to Induce Neuroendocrine Prostate Cancer.Cancer research · 2021Article
- Wnt/β-catenin signaling: Structure, assembly and endocytosis of the signalosome.Development, growth & differentiation · 2021Review
- Can We Pharmacologically Target Dishevelled: The Key Signal Transducer in the Wnt Pathways?Handbook of experimental pharmacology · 2021Article
- Primary Cilia Formation Does Not Rely on WNT/β-Catenin Signaling.Frontiers in cell and developmental biology · 2021Article
- Intersection of two key signal integrators in the cell: activator of G-protein signaling 3 and dishevelled-2.Journal of cell science · 2020Article
- Wnt regulation: exploring Axin-Disheveled interactions and defining mechanisms by which the SCF E3 ubiquitin ligase is recruited to the destruction complex.Molecular biology of the cell · 2020Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Dishevelled (Dvl) proteins are intracellular effectors of Wnt signaling that have essential roles in both canonical and noncanonical Wnt pathways. It has long been known that Wnts stimulate Dvl phosphorylation, but relatively little is known about its functional significance. We have previously reported that both Wnt3a and Wnt5a induce Dvl2 phosphorylation that is associated with an electrophoretic mobility shift and loss of recognition by monoclonal antibody 10B5. In the present study, we mapped the 10B5 epitope to a 16-amino acid segment of human Dvl2 (residues 594-609) that contains four Ser/Thr residues. Alanine substitution of these residues (P4m) eliminated the mobility shift induced by either Wnt3a or Wnt5a. The Dvl2 P4m mutant showed a modest increase in canonical Wnt/β-catenin signaling activity relative to wild type. Consistent with this finding, Dvl2 4Pm preferentially localized to cytoplasmic puncta. In contrast to wild-type Dvl2, however, the P4m mutant was unable to rescue Wnt3a-dependent neurite outgrowth in TC-32 cells following suppression of endogenous Dvl2/3. Earlier work has implicated casein kinase 1δ/ε as responsible for the Dvl mobility shift, and a CK1δ in vitro kinase assay confirmed that Ser(594), Thr(595), and Ser(597) of Dvl2 are CK1 targets. Alanine substitution of these three residues was sufficient to abrogate the Wnt-dependent mobility shift. Thus, we have identified a cluster of Ser/Thr residues in the C-terminal domain of Dvl2 that are Wnt-induced phosphorylation (WIP) sites. Our results indicate that phosphorylation at the WIP sites reduces Dvl accumulation in puncta and attenuates β-catenin signaling, whereas it enables noncanonical signaling that is required for neurite outgrowth.
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