Affinage

DVL1

Segment polarity protein dishevelled homolog DVL-1 · UniProt O14640

Length
695 aa
Mass
75.2 kDa
Annotated
2026-06-09
46 papers in source corpus 22 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DVL1 is a multifunctional Dishevelled-family scaffold protein that transduces Wnt signals through both canonical (β-catenin-dependent) and non-canonical (planar cell polarity/JNK) branches, and additionally functions as a nuclear transcriptional regulator (PMID:12556519, PMID:21316586, PMID:27500936). In the canonical cytoplasmic pathway, casein kinase I epsilon (CSNK1E/CKIε) phosphorylates DVL1 and enhances its binding to Frat-1 (via residues 228–250), a complex required for Wnt-3a-induced β-catenin accumulation and TCF-dependent transcription (PMID:12556519); the DIX domain of DVL1 forms a stable complex with the DIX domain of Axin1 (PMID:20846493). Its level and signaling output are tuned by multiple regulators: HECW1 ubiquitinates DVL1 to promote its degradation and restrain Wnt/β-catenin signaling (PMID:38266865), DACT3 binds DVL1 to suppress GSK-3β/β-catenin phosphorylation and downstream transcription (PMID:40838391), neuroglobin drives its proteasomal degradation (PMID:30041403), and Nup358 binding suppresses DVL1 phase separation into condensates that otherwise promote Tankyrase-mediated Axin1 degradation and ligand-independent Wnt activation (PMID:41929184). In non-canonical signaling, DVL1 hyperphosphorylates Frizzled3 and blocks its internalization to control PCP-dependent commissural axon guidance (PMID:21316586). Independently of receptor signaling, DVL1 enters the nucleus, accumulates at rDNA loci to repress RNA Pol I transcription by displacing SIRT7 (PMID:27500936), binds gene promoters in a manner regulated by lysine acetylation at K69 and K285 (PMID:31700102), and drives proliferation in myoblasts and rhabdomyosarcoma cells without requiring increased nuclear β-catenin (PMID:35589804). De novo C-terminal frameshift variants in DVL1 cause autosomal-dominant Robinow syndrome: these mutants are trapped in cytoplasmic puncta unresponsive to Wnt ligand, lose canonical and gain non-canonical Wnt activity, and produce skeletal and tissue dysmorphogenesis through JNK and BMP pathway activation (PMID:25817016, PMID:25817014, PMID:36916233, PMID:40600289). In knockout mice, DVL1 is required for normal social behavior and sensorimotor gating and for gut homeostasis across epithelial and immune compartments (PMID:9298901, PMID:14960015, PMID:27525310).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1997 High

    Established that DVL1 has a non-redundant physiological role in the CNS, answering whether this Wnt transducer matters at the organismal level despite paralog redundancy.

    Evidence Germline Dvl1 knockout mice with behavioral assays (social dominance, PPI of startle)

    PMID:14960015 PMID:9298901

    Open questions at the time
    • Molecular basis linking DVL1 loss to social/sensorimotor deficits not defined
    • Cell types and circuits responsible unidentified
  2. 1999 Medium

    Identified a DVL1 PDZ-domain interaction with the EGFR substrate EPS8 and reciprocal phosphorylation regulation, hinting at crosstalk between DVL1 and tyrosine-kinase signaling.

    Evidence Yeast two-hybrid, in vitro binding, co-transfection phosphorylation assays

    PMID:10581192

    Open questions at the time
    • Functional consequence of DVL1–EPS8 crosstalk in Wnt signaling unclear
    • Single lab, no in vivo validation
  3. 2003 High

    Defined how CSNK1E phosphorylation couples DVL1 to canonical Wnt output, showing the CKIε–DVL1–Frat-1 module is required for β-catenin accumulation and TCF transcription.

    Evidence Co-IP, deletion mutagenesis (Δ228–250), CKIε RNAi, TOPFlash reporter, β-catenin assays in L and HEK293 cells

    PMID:12556519

    Open questions at the time
    • Phosphosite map on DVL1 not resolved
    • Structural basis of Frat-1 binding unknown
  4. 2010 Medium

    Demonstrated direct DIX–DIX assembly between DVL1 and Axin1, providing a biochemical basis for the destruction-complex regulatory interface.

    Evidence Multi-cistronic E. coli co-expression, affinity and size-exclusion chromatography, preliminary crystallization

    PMID:20846493

    Open questions at the time
    • No mutagenesis or functional validation of the interface
    • Crystal structure not solved
  5. 2011 High

    Showed DVL1 acts in non-canonical PCP signaling by hyperphosphorylating Frizzled3 and blocking its internalization, establishing a receptor-trafficking control point for directional Wnt sensing in axon guidance.

    Evidence PCP-component genetic loss-of-function, phosphorylation/internalization assays, growth cone imaging, Wnt5a axon guidance assays

    PMID:21316586

    Open questions at the time
    • Kinase mediating Frizzled3 phosphorylation not identified
    • DVL1 vs paralog specificity in PCP not fully resolved
  6. 2015 Medium

    Linked DVL1 to a human Mendelian disease, establishing that C-terminal frameshift variants escaping NMD cause autosomal-dominant Robinow syndrome via altered Wnt signaling.

    Evidence Whole-exome/Sanger sequencing, trio analysis, patient transcript analysis; TOPFlash assays with mutant and mutant+WT co-expression and GFP stability

    PMID:25817014 PMID:25817016

    Open questions at the time
    • Functional mechanism inferred rather than reconstituted in the original reports
    • Connection of TOPFlash gain-of-function to osteosclerosis not directly tested
  7. 2016 High

    Uncovered an unexpected nuclear function: DVL1 represses RNA Pol I rDNA transcription downstream of Wnt5a by binding rDNA chromatin and displacing the activator SIRT7.

    Evidence DVL1-specific siRNA, ChIP for DVL1 and SIRT7 at rDNA, Pol I transcription assays, NOR imaging in breast cancer cells

    PMID:27500936

    Open questions at the time
    • Mechanism of DVL1 nuclear import/rDNA targeting unknown
    • Whether SIRT7 release is direct displacement unresolved
  8. 2016 High

    Defined a dual epithelial and immune requirement for DVL1 in gut homeostasis, showing Paneth cell and T-cell defects combine to drive GI dysfunction.

    Evidence Dvl1 knockout mice, bone marrow chimeras, transit/Paneth/CD8 readouts, microbiota manipulation

    PMID:27525310

    Open questions at the time
    • Wnt-pathway dependence of the gut phenotype not dissected
    • Cell-intrinsic molecular targets unidentified
  9. 2018 Medium

    Identified post-translational and nuclear-transcriptional control of DVL1: neuroglobin-driven proteasomal degradation suppresses Wnt output, while nuclear DVL1 binds CYP19A1 promoters to control aromatase and estrogen production.

    Evidence Co-IP, proteasome inhibitor and TOPFlash assays (neuroglobin); ChIP and siRNA with aromatase/E2 readouts (CYP19A1)

    PMID:30041403 PMID:30479694

    Open questions at the time
    • E3 ligase mediating neuroglobin-dependent degradation not identified
    • Direct vs indirect promoter regulation by DVL1 unclear
  10. 2019 Medium

    Showed that lysine acetylation at K69 (DIX) and K285 (PDZ) governs DVL1 nuclear localization and promoter binding, defining a PTM switch for its transcriptional role.

    Evidence LC-MS/MS acetyl-site mapping, acetyl-mimetic/deficient mutants, fractionation/IF, ChIP in TNBC cells

    PMID:31700102

    Open questions at the time
    • Acetyltransferase/deacetylase enzymes unidentified
    • Single lab
  11. 2021 Medium

    Genome-wide profiling positioned nuclear DVL1 as a chromatin-associated regulator whose binding sites overlap H3K27me3/EZH2 repressive marks.

    Evidence DVL-1 ChIP-Seq with co-localization analysis against H3K27me3/EZH2 datasets

    PMID:34659647

    Open questions at the time
    • Direct DVL1–PRC2 interaction not demonstrated
    • Limited functional follow-up
  12. 2022 Medium

    Established that DVL1's nuclear pro-proliferative function is β-catenin-independent and uses domain requirements distinct from DVL3, dissociating its growth role from canonical Wnt output.

    Evidence siRNA, nuclear/cytoplasmic fractionation, domain-deletion constructs, proliferation assays in myoblasts and rhabdomyosarcoma cells

    PMID:35589804

    Open questions at the time
    • Nuclear effectors of DVL1-driven proliferation unknown
    • Domain element required for DVL1 (vs DVL3) not pinpointed
  13. 2023 Medium

    Expanded DVL1's regulatory reach to GPCR turnover, showing it targets Sstr2 for lysosomal degradation and selectively dampens agonist-stimulated ERK signaling in a Wnt-modulated manner.

    Evidence Co-IP, lysosomal inhibitor, internalization/recycling, adenylyl cyclase and ERK1/2 assays, Wnt overexpression/inhibitor experiments in NET cells

    PMID:36965619

    Open questions at the time
    • Structural basis of DVL1–Sstr2 binding unknown
    • Generality across other GPCRs untested
  14. 2023 Medium

    Mechanistically connected Robinow variants to pathway rewiring, showing they lose canonical and gain non-canonical Wnt activity and produce skeletal/wing dysmorphology in chicken and Drosophila.

    Evidence Transient WT/variant DVL1 expression in Drosophila and chicken with Wnt reporters and morphological analysis; localization, TOPFlash, and CSNK1E phosphorylation assays (preprint)

    PMID:36916233 PMID:bio_10.1101_2025.08.02.668297

    Open questions at the time
    • Why mutant C-terminus traps DVL1 in puncta not structurally defined
    • CSNK1E-phosphorylation interference mechanism unresolved
  15. 2024 Medium

    Identified HECW1 as an E3 ligase that ubiquitinates and degrades DVL1, defining a degradation node that restrains Wnt/β-catenin-driven proliferation in cervical cancer.

    Evidence Ubiquitination assay, Western blot, nuclear β-catenin fractionation, TOPFlash, siRNA, in vivo tumor assay

    PMID:38266865

    Open questions at the time
    • Ubiquitin chain type and DVL1 acceptor sites not mapped
    • Upstream regulation of HECW1 activity unknown
  16. 2025 Medium

    Resolved additional layers of DVL1 control: DACT3 binding suppresses GSK-3β/β-catenin phosphorylation, and Nup358 binding prevents DVL1 phase separation into condensates that otherwise drive Tankyrase-mediated Axin1 degradation and ligand-independent Wnt activation.

    Evidence Co-IP, Western blot, TOPFlash, functional assays in NSCLC (DACT3); conditional Nup358 knockout mice, co-IP, phase-separation and Axin1 degradation assays, Tankyrase inhibitor, crypt histology (Nup358, preprint)

    PMID:40838391 PMID:41929184

    Open questions at the time
    • Physiological conditions triggering DVL1 condensation not defined
    • Whether DACT3 and Nup358 control converge mechanistically untested
  17. 2025 Medium

    Detailed the tissue-level pathology of Robinow variants, showing JNK-dependent ectopic MMP1, caspase-dependent cell death, collagen IV accumulation, and elevated BMP signaling underlie dysmorphogenesis.

    Evidence Drosophila DVL1-1519ΔT expression, caspase inhibitor rescue, MMP1/Viking staining, JNK epistasis, dad-lacZ BMP reporter

    PMID:40600289

    Open questions at the time
    • Direct molecular target of variant DVL1 driving JNK/BMP activation unknown
    • Relevance to human skeletal phenotype not directly established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DVL1's nuclear transcriptional/rDNA-repressive functions are mechanistically integrated with its cytoplasmic Wnt-scaffold role, and what governs its nuclear import and phase behavior in vivo, remain unresolved.
  • No structural model of full-length DVL1 in distinct compartments
  • Nuclear import machinery and condensation triggers undefined
  • Paralog-specific functional division (DVL1 vs DVL2/DVL3) incompletely mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 4 GO:0003677 DNA binding 3 GO:0060090 molecular adaptor activity 3 GO:0060089 molecular transducer activity 2
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 3 GO:0000228 nuclear chromosome 1 GO:0005730 nucleolus 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3
Partners
AXIN1CSNK1EDACT3EPS8FRAT1FZD3HECW1SSTR2

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Dvl1 knockout mice are viable and fertile but exhibit specific behavioral phenotypes including reduced social interaction and deficits in sensorimotor gating (prepulse inhibition), establishing that Dvl1 is required for normal social behavior and sensorimotor processing in the central nervous system. Gene targeting/knockout mouse, behavioral assays (social dominance, nest-building, huddling, PPI of acoustic/tactile startle) Cell High 14960015 9298901
2003 CKI epsilon (casein kinase I epsilon) phosphorylates Dvl-1 and enhances its binding to Frat-1; the amino acid region 228–250 of Dvl-1 is necessary for binding Frat-1. This complex is required for Wnt-3a-induced accumulation of beta-catenin and activation of TCF-4-dependent transcription. Co-immunoprecipitation, deletion mutagenesis (Dvl-1 Δ228–250), RNAi knockdown of CKI epsilon, TOPFlash/TCF-4 luciferase reporter assay, beta-catenin accumulation assay in L cells and HEK293 cells The Journal of biological chemistry High 12556519
2011 DVL1 promotes hyperphosphorylation of Frizzled3 and prevents its internalization, thereby inhibiting planar cell polarity (PCP) signaling in commissural axon growth cones. Vangl2 antagonizes this by reducing Frizzled3 phosphorylation and promoting its internalization, sharpening PCP signaling at filopodia tips for directional Wnt sensing. Genetic loss-of-function (PCP component knockouts/mutants), phosphorylation assays, internalization assays, immunolocalization in commissural axon growth cones, axon guidance assays (Wnt5a-stimulated outgrowth and A-P guidance) Developmental cell High 21316586
1999 EPS8 (a substrate of activated EGF receptor) physically interacts with the PDZ domain of Dvl1. In the presence of EPS8, Dvl1 becomes hyperphosphorylated; conversely, Dvl1 inhibits EGF receptor-induced tyrosine phosphorylation of EPS8. Yeast two-hybrid screening, in vitro binding confirmation, co-transfection/phosphorylation assays, immunohistochemistry showing overlapping expression Biochemical and biophysical research communications Medium 10581192
2010 The DIX domain of DVL1 physically interacts with the DIX domain of Axin1 to form a stable complex; co-expression of both DIX domains in a multi-cistronic system stabilizes the otherwise unstable individual DIX domain fragments, enabling complex formation confirmed by affinity chromatography and size-exclusion chromatography. Multi-cistronic co-expression in E. coli, affinity chromatography, size-exclusion chromatography (SEC), preliminary crystallization of DIX(Dvl1)–DIX(Axin1) complex BMB reports Medium 20846493
2016 Wnt5a signals specifically through DVL1 to repress ribosomal DNA (rDNA) transcription by RNA polymerase I in breast cancer cells. DVL1 accumulates in nucleolar organizer regions (NORs) and binds rDNA chromatin; upon DVL1 binding, the Pol I transcription activator SIRT7 is released from rDNA loci coincident with disassembly of Pol I transcription machinery at the rDNA promoter. siRNA knockdown of DVL1 (specificity established vs. DVL2/DVL3), chromatin immunoprecipitation (ChIP) for DVL1 binding to rDNA, Pol I transcription assays, SIRT7 ChIP, live-cell imaging/microscopy of DVL1 at NORs, Wnt5a treatment assays PLoS genetics High 27500936
2015 De novo heterozygous frameshift mutations in DVL1 exon 14 (penultimate exon) cause autosomal-dominant Robinow syndrome. Mutant transcripts escape nonsense-mediated decay and are predicted to generate C-terminally truncated proteins with a distinct -1 reading-frame terminus, implicating loss/alteration of the DVL1 C-terminal domain in non-canonical Wnt-5a pathway disruption. Whole-exome sequencing, Sanger sequencing, transcript analysis from patient leukocytes confirming NMD escape and expression of both alleles, de novo mutation verification in parent–proband trios American journal of human genetics Medium 25817016
2015 De novo DVL1 frameshift mutations that delete the C-terminus and replace it with a novel highly basic sequence cause Robinow syndrome with osteosclerosis (RS-OS). In vitro TOPFlash assays showed the mutant allele alone was less active than wild-type in canonical Wnt signaling, but co-expression of mutant and wild-type alleles produced ~2-fold higher canonical Wnt activity than wild-type alone, suggesting a dominant gain-of-function interaction that may underlie the osteosclerotic phenotype. Whole-exome sequencing, GFP-tagged construct transfection showing unimpaired protein stability, TOPFlash canonical Wnt reporter assay with mutant alone and mutant+WT co-expression, fibroblast transcript analysis American journal of human genetics Medium 25817014
2019 DVL-1 is acetylated on at least 12 lysine residues; acetylation of two key residues, K69 (DIX domain) and K285 (PDZ domain), promotes nuclear over cytoplasmic localization of DVL-1 and influences its binding to gene promoters and regulation of cancer-related genes in triple-negative breast cancer cells. LC-MS/MS identification of acetylation sites, site-directed mutagenesis (acetylation-mimetic/deficient mutants), subcellular fractionation and immunofluorescence localization, chromatin immunoprecipitation (ChIP) for promoter binding Scientific reports Medium 31700102
2021 DVL-1 localizes to the nucleus in breast cancer cells and binds genomic regions including CYP19A1 promoters. DVL-1 peaks co-localize with H3K27me3 and EZH2 repressive chromatin marks, identifying DVL-1 as a transcriptional regulator with an epigenetic association. ChIP-Seq genome-wide profiling of DVL-1 binding sites, co-localization analysis with H3K27me3 and EZH2 ChIP-Seq datasets Genes & cancer Medium 34659647
2018 DVL-1 and DVL-3 enter the nucleus and localize to at least two breast-cancer-associated CYP19A1 promoters (pII and I.4) and a distal placental promoter (I.1). Loss of DVL-1 function leads to differential changes in aromatase transcript levels and in estrogen (E2) production in breast cancer cells. ChIP (DVL localization to CYP19A1 promoters), siRNA knockdown of DVL-1 and DVL-3, aromatase transcript quantification, E2 production measurement Oncotarget Medium 30479694
2018 Neuroglobin directly interacts with DVL-1 (Dishevelled-1) and promotes its proteasomal degradation. Neuroglobin overexpression inhibits DVL-1-mediated TCF/LEF (TOPFlash) reporter activity and beta-catenin expression, and also enhances TNF-alpha-induced NFκB activation through DVL-1 downregulation. Yeast two-hybrid (prior study cited), co-immunoprecipitation confirming interaction, co-localization by immunofluorescence, proteasome inhibitor experiments, TOPFlash luciferase reporter assay, MTT cell viability assay International journal of molecular sciences Medium 30041403
2022 DVL1 and DVL3 must be present in the nucleus to regulate proliferation in human myoblasts and rhabdomyosarcoma cells, operating through different domain requirements: DVL3 requires DIX and PDZ domains, while DVL1 does not. DVL1 and DVL3 regulate proliferation independently of markedly increased nuclear beta-catenin translocation. siRNA knockdown of DVL1 and DVL3, nuclear/cytoplasmic fractionation, domain-deletion constructs, proliferation and differentiation assays, beta-catenin localization analysis Scientific reports Medium 35589804
2023 DVL1 interacts with somatostatin receptor 2 (Sstr2) in a ligand-independent manner and targets Sstr2 for lysosomal degradation. This interaction does not affect receptor internalization, recycling, or adenylyl cyclase signaling but suppresses agonist-stimulated ERK1/2 activation. Wnt overexpression potentiates DVL1-dependent Sstr2 degradation, and Wnt pathway inhibitors boost Sstr2 expression in neuroendocrine tumor cells. Co-immunoprecipitation (DVL1–Sstr2 interaction), lysosomal inhibitor assays, receptor internalization/recycling assays, adenylyl cyclase signaling assay, ERK1/2 phosphorylation assay, Wnt overexpression and pathway inhibitor treatment experiments The Journal of biological chemistry Medium 36965619
2016 Dvl1 has a dual epithelial and immune cell function required for normal gut homeostasis. Dvl1-/- mice show increased gut transit time, mislocalization of Paneth cells, and increased CD8+ T cells. Bone marrow chimera experiments established that GI dysfunction requires abnormalities in both epithelial and immune compartments. Gut microbiota manipulation rescued transit abnormality without correcting cellular defects. Dvl1 germline knockout mice, bone marrow chimera experiments, gut transit time measurement, Paneth cell localization, CD8+ T cell quantification, microbiota manipulation/transplantation JCI insight High 27525310
2023 DVL1 Robinow syndrome frameshift variants (acting as a prototype: DVL1-1519ΔT) cause loss of canonical Wnt signaling and gain of non-canonical Wnt signaling in chicken and Drosophila developmental assays. Expression of variant DVL1 in Drosophila wings and chicken produced major disorganization of cartilage and wing morphology compared to wild-type DVL1. Transient expression of human WT and variant DVL1 in Drosophila and chicken embryo models, canonical Wnt reporter assays, non-canonical Wnt pathway readouts, morphological phenotype analysis Disease models & mechanisms Medium 36916233
2023 DVL1 Robinow syndrome frameshift variants fail to redistribute from cytoplasmic puncta to respond to Wnt ligand stimulation (unlike wild-type DVL1), fail to activate canonical Wnt signaling in TOPFlash assays, and the mutant C-terminal tail interferes with CSNK1E (casein kinase 1 epsilon)-induced phosphorylation of DVL1. Immunocytochemistry of DVL1 localization in response to Wnt ligands, TOPFlash canonical Wnt reporter assay, CSNK1E co-transfection phosphorylation assay; WT, frameshift, and truncated constructs of DVL1-3 compared bioRxivpreprint Medium bio_10.1101_2025.08.02.668297
2024 HECW1 (E3 ubiquitin ligase) promotes ubiquitination and degradation of DVL1, thereby restraining DVL1-mediated Wnt/β-catenin signaling. Inhibition of HECW1 reduced DVL1 ubiquitination and upregulated DVL1 protein, promoting nuclear β-catenin accumulation and cell proliferation in cervical cancer cells. Ubiquitination assay (DVL1 ubiquitination with HECW1 modulation), Western blot for DVL1 protein levels, nuclear β-catenin fractionation, TOPFlash/TCF-LEF luciferase assay, siRNA knockdown of HECW1 and DVL1, in vivo tumor formation assay Experimental cell research Medium 38266865
2025 DACT3 directly interacts with DVL1 (confirmed by co-immunoprecipitation) and inhibits DVL1-induced activation of canonical Wnt signaling. The DACT3–DVL1 interaction inhibits phosphorylation of GSK-3β at serine 9 and β-catenin at serine 675, thereby reducing β-catenin nuclear translocation and downstream transcription. DACT3 suppresses DVL1-driven invasion, proliferation, migration, and cisplatin resistance in NSCLC cells. Co-immunoprecipitation (DACT3–DVL1 interaction), Western blot (GSK-3β pS9, β-catenin pS675, nuclear β-catenin), TOPFlash luciferase reporter assay, siRNA/cDNA transfection loss/gain of function, immunofluorescence, cell invasion/proliferation/migration assays, in vivo tumorigenesis FASEB journal Medium 40838391
2025 Dvl1 DVL1 Robinow syndrome variants disrupt epithelial imaginal disc morphology in Drosophila with increased cell death (caspase-dependent) and without changes in cell proliferation; they also cause ectopic MMP1 expression and tissue distortion dependent on JNK signaling, and abnormal accumulation of collagen IV (Viking) in pupal wings, as well as elevated BMP signaling. Drosophila expression of DVL1 variant (DVL1-1519ΔT), immunofluorescence, caspase inhibitor rescue, MMP1 immunostaining, JNK pathway genetic epistasis, dad-lacZ BMP reporter, Viking (collagen IV) staining in pupal wings Developmental dynamics Medium 40600289
2025 Nup358 interacts with Dvl1 through its N-terminal domain and inhibits Dvl1 spontaneous phase separation (condensate/biomolecular condensate formation). In the absence of Nup358, Dvl1 forms condensates that promote Tankyrase-mediated degradation of Axin1, leading to constitutive β-catenin stabilization and ligand-independent Wnt activation, depleting the transit-amplifying progenitor compartment in intestinal crypts. Conditional Nup358 knockout in adult mice, co-immunoprecipitation (Nup358–Dvl1 interaction), domain-mapping (N-terminal domain of Nup358), phase separation/condensate assays, Axin1 degradation assay, Tankyrase inhibitor experiments, intestinal crypt histology and ISC/TA compartment analysis bioRxivpreprint Medium 41929184

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 Social interaction and sensorimotor gating abnormalities in mice lacking Dvl1. Cell 378 9298901
2011 Vangl2 promotes Wnt/planar cell polarity-like signaling by antagonizing Dvl1-mediated feedback inhibition in growth cone guidance. Developmental cell 163 21316586
2015 DVL1 frameshift mutations clustering in the penultimate exon cause autosomal-dominant Robinow syndrome. American journal of human genetics 111 25817016
2003 Amplification, up-regulation and over-expression of DVL-1, the human counterpart of the Drosophila disheveled gene, in primary breast cancers. Cancer science 105 12824876
2003 Casein kinase I epsilon enhances the binding of Dvl-1 to Frat-1 and is essential for Wnt-3a-induced accumulation of beta-catenin. The Journal of biological chemistry 96 12556519
2004 Expanded characterization of the social interaction abnormalities in mice lacking Dvl1. Genes, brain, and behavior 78 14960015
2015 Mutations in DVL1 cause an osteosclerotic form of Robinow syndrome. American journal of human genetics 69 25817014
2003 Up-regulation and overproduction of DVL-1, the human counterpart of the Drosophila dishevelled gene, in cervical squamous cell carcinoma. Oncology reports 59 12883684
2021 FUBP1 promotes colorectal cancer stemness and metastasis via DVL1-mediated activation of Wnt/β-catenin signaling. Molecular oncology 44 34288405
2018 DVL1 and DVL3 differentially localize to CYP19A1 promoters and regulate aromatase mRNA in breast cancer cells. Oncotarget 41 30479694
2005 Upregulation and overexpression of DVL1, the human counterpart of the Drosophila dishevelled gene, in prostate cancer. Tumori 40 16457155
2014 Brain metastases from lung cancer show increased expression of DVL1, DVL3 and beta-catenin and down-regulation of E-cadherin. International journal of molecular sciences 38 24933634
2019 Acetylation of conserved DVL-1 lysines regulates its nuclear translocation and binding to gene promoters in triple-negative breast cancer. Scientific reports 33 31700102
2020 DKK3 attenuates JNK and AP-1 induced inflammation via Kremen-1 and DVL-1 in mice following intracerebral hemorrhage. Journal of neuroinflammation 26 32331523
2023 circMMD reduction following tumor treating fields inhibits glioblastoma progression through FUBP1/FIR/DVL1 and miR-15b-5p/FZD6 signaling. Journal of experimental & clinical cancer research : CR 22 36932454
2016 Wnt5a Signals through DVL1 to Repress Ribosomal DNA Transcription by RNA Polymerase I. PLoS genetics 21 27500936
2018 Different behaviour of DVL1, DVL2, DVL3 in astrocytoma malignancy grades and their association to TCF1 and LEF1 upregulation. Journal of cellular and molecular medicine 18 30468298
1999 Identification of EPS8 as a Dvl1-associated molecule. Biochemical and biophysical research communications 17 10581192
2022 DVL1 and DVL3 require nuclear localisation to regulate proliferation in human myoblasts. Scientific reports 14 35589804
2021 Genomic profiling of DVL-1 and its nuclear role as a transcriptional regulator in triple negative breast cancer. Genes & cancer 14 34659647
2013 Significant overexpression of DVL1 in Taiwanese colorectal cancer patients with liver metastasis. International journal of molecular sciences 13 24129181
2016 Dual epithelial and immune cell function of Dvl1 regulates gut microbiota composition and intestinal homeostasis. JCI insight 12 27525310
2018 Neuroglobin Regulates Wnt/β-Catenin and NFκB Signaling Pathway through Dvl1. International journal of molecular sciences 11 30041403
2023 Mechanistic studies in Drosophila and chicken give new insights into functions of DVL1 in dominant Robinow syndrome. Disease models & mechanisms 9 36916233
2024 HECW1 restrains cervical cancer cell growth by promoting DVL1 ubiquitination and downregulating the activation of Wnt/β-catenin signaling. Experimental cell research 8 38266865
2022 A novel frameshift mutation of DVL1-induced Robinow syndrome: A case report and literature review. Molecular genetics & genomic medicine 8 35137569
2023 SPATA2 suppresses epithelial-mesenchymal transition to inhibit metastasis and radiotherapy sensitivity in non-small cell lung cancer via impairing DVL1/β-catenin signaling. Thoracic cancer 7 36814090
2023 MiR-1281 is involved in depression disorder and the antidepressant effects of Kai-Xin-San by targeting ADCY1 and DVL1. Heliyon 7 36938448
2016 The expression of SFRP1, SFRP3, DVL1, and DVL2 proteins in testicular germ cell tumors. APMIS : acta pathologica, microbiologica, et immunologica Scandinavica 7 27599467
2023 Hyperoxia exposure upregulates Dvl-1 and activates Wnt/β-catenin signaling pathway in newborn rat lung. BMC molecular and cell biology 5 36726071
2010 Coexpression and protein-protein complexing of DIX domains of human Dvl1 and Axin1 protein. BMB reports 5 20846493
2021 Decoding the Role of DVL1 in Intracranial Meningioma. International journal of molecular sciences 4 34769425
2015 Expression of DDR1 and DVL1 in invasive ductal and lobular breast carcinoma does not correlate with histological type, grade and hormone receptor status. Asian Pacific journal of cancer prevention : APJCP 4 25824769
2023 The Wnt pathway protein Dvl1 targets somatostatin receptor 2 for lysosome-dependent degradation. The Journal of biological chemistry 3 36965619
2021 Dishevelled family proteins (DVL1-3) expression in intrauterine growth restriction (IUGR) placentas. Bosnian journal of basic medical sciences 3 33485290
2014 Dishevelled-1 (Dvl-1) protein: a potential participant of oxidative stress induced by selenium deficiency. Biological trace element research 3 24234591
2013 Rare missense variants in DVL1, one of the human counterparts of the Drosophila dishevelled gene, do not confer increased risk for neural tube defects. Birth defects research. Part A, Clinical and molecular teratology 3 23836490
2024 The LncRNA6524/miR-92a-2-5p/Dvl1/Wnt/β-catenin axis promotes renal fibrosis in the UUO mouse model. Archives of biochemistry and biophysics 2 39389150
2024 Expression of Wnt signaling proteins LEF1, β-catenin, GSK3β, DVL1, and N-myc varies across retinoblastoma subtypes and pRb phosphorylation status. Scientific reports 2 39738380
2025 DACT3-DVL1 Interaction-Mediated Canonical WNT Signaling Regulates Non-Small Cell Lung Cancer Progression and Cisplatin Resistance. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1 40838391
2024 Exploration and identification of diabetes targets in nursing: CDH1 and DVL1. Medicine 1 39495995
2026 Nup358 Sustains Intestinal Epithelial Homeostasis by Preventing Dvl1 Condensate Formation to Restrain Wnt Signaling. bioRxiv : the preprint server for biology 0 41929184
2026 miR-1247-5p is correlated with cervical cancer and regulates cervical cancer cell functions by targeting DVL1. Nucleosides, nucleotides & nucleic acids 0 42033419
2025 Sp2 Transcription Factor Alleviates Chondrocyte Loss in Osteoarthritis by Repressing the DVL1-Dependent Wnt/β-Catenin Signaling Pathway. The journal of gene medicine 0 40420355
2025 Robinow syndrome DVL1 variants disrupt morphogenesis and appendage formation in a Drosophila disease model. Developmental dynamics : an official publication of the American Association of Anatomists 0 40600289
2024 Evaluation of LRP6, SFRP3, and DVL1 Protein Concentrations in Serum of Patients with Gastroenteropancreatic or Bronchopulmonary Neuroendocrine Tumors. Cancers 0 39796676

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