Affinage

DVL3

Segment polarity protein dishevelled homolog DVL-3 · UniProt Q92997

Length
716 aa
Mass
78.1 kDa
Annotated
2026-06-09
41 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DVL3 is a cytoplasmic scaffold protein that relays WNT signals from Frizzled (FZD) receptors to both canonical (β-catenin) and non-canonical (planar cell polarity) effectors (PMID:42127203, PMID:39094673). WNT stimulation drives CK1-mediated multiphosphorylation of DVL3, triggering an intramolecular phospho-switch between the DEP domain and the adjacent disordered region that is mutually exclusive with Frizzled association; charge accumulation near the DEP domain is required for canonical Wnt/β-catenin signaling, and FZD receptors are prominent effectors of this switch (PMID:42127203). In the non-canonical arm, WNT5B-FZD3 recruits DVL3 to the plasma membrane through its DEP domain, where DVL3 activates RAC1 and downstream JNK signaling (PMID:39094673). DVL3 functions as a positive regulator of Wnt/β-catenin in multiple contexts, recruiting IPMK to the membrane via its PDZ domain and proline-rich tail (PMID:22940627) and acting as a node whose abundance is tuned by degradation: the autophagy scaffold ALFY selectively clears DVL3 aggregates (PMID:27008544), while AMPK/mTOR signaling and ubiquitin/proteasomal degradation lower DVL3 protein levels (PMID:23301094). Beyond the membrane, DVL3 translocates to the nucleus, localizing to CYP19A1 (aromatase) promoters to control transcription and estradiol production (PMID:30479694) and driving proliferation in a manner dependent on its DIX and PDZ domains (PMID:35589804). DVL3 also participates in non-Wnt signaling, residing in an IGFIR-Shc-Grb2-SOS-DAB2 adaptor complex that links IGF signaling to RAS/MEK-ERK (PMID:25168481) and restraining NF-κB-driven inflammatory cytokine production downstream of TLR4/Wnt3a (PMID:31884387). Pathogenic DVL3 frameshifting variants causing Robinow syndrome generate a novel basic C-terminus that interferes with CSNK1E-induced phosphorylation and abolishes WNT-induced membrane redistribution and canonical signaling [PMID:bio_10.1101_2025.08.02.668297].

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 1997 High

    Established the molecular identity of human DVL3 as a Dishevelled homolog, providing the foundation for studying it as a WNT pathway component.

    Evidence cDNA cloning, sequencing, and chromosomal mapping to 3q27

    PMID:9344861

    Open questions at the time
    • No functional or mechanistic assignment beyond homology
    • Domain-level activities not characterized
  2. 2012 Medium

    Showed DVL3 acts as a membrane-recruitment scaffold, defining how it propagates canonical Wnt signals by relocating an effector kinase.

    Evidence Co-IP, domain deletion mutants, and fractionation/imaging after Wnt3a stimulation; IPMK translocation

    PMID:22940627

    Open questions at the time
    • Direct vs. indirect PDZ-mediated IPMK binding not resolved
    • Single lab
  3. 2014 High

    Placed DVL3 outside the canonical Wnt axis as a component of an IGFIR-to-RAS adaptor complex, revealing a non-redundant scaffolding role in growth-factor signaling.

    Evidence Genetic screen, Co-IP of DVL3-Shc-Grb2-SOS-DAB2, siRNA, xenograft, MEK-ERK assays

    PMID:25168481

    Open questions at the time
    • Direct binding partner of DVL3 within the complex not pinpointed
    • Mechanism of ERK suppression unclear
  4. 2016 High

    Defined a DVL3-specific degradation route, explaining how cellular DVL3 abundance and Wnt output are controlled in development.

    Evidence Human exome sequencing, Drosophila model, autophagy inhibition, isoform-specific knockdowns

    PMID:27008544

    Open questions at the time
    • Molecular basis of ALFY isoform selectivity for DVL3 unknown
    • Aggregate recognition signal not defined
  5. 2018 Medium

    Demonstrated a nuclear function for DVL3, expanding its role from cytoplasmic scaffold to direct chromatin-associated transcriptional regulator.

    Evidence ChIP at CYP19A1 promoters, DVL knockdown, transcript and estradiol quantification

    PMID:30479694

    Open questions at the time
    • Nuclear import mechanism not defined
    • DNA-binding partners at promoters unidentified
  6. 2019 Medium

    Linked DVL3 to cytoskeletal organization and to inflammatory tone, broadening its functional repertoire beyond β-catenin transcription.

    Evidence RNAi knockdown in Sertoli cells/testis (cytoskeleton, tight junctions); gain/loss-of-function and endotoxin model (NF-κB restraint)

    PMID:30808893 PMID:31884387

    Open questions at the time
    • Direct molecular targets in cytoskeletal regulation unknown
    • Mechanism by which DVL3/β-catenin restrains NF-κB not detailed
  7. 2022 Medium

    Tied DVL3 nuclear localization to a proliferation function dependent on specific domains, distinguishing it from DVL1 and from bulk β-catenin translocation.

    Evidence Domain mutants, nuclear imaging, proliferation assays in myoblasts; Co-IP of MEX3A-DVL3 in endometrial carcinoma

    PMID:35589804 PMID:36614043

    Open questions at the time
    • β-catenin-independent proliferation mechanism not defined
    • Functional consequence of MEX3A binding on DVL3 itself unclear
  8. 2024 Medium

    Identified a redox post-translational modification and a membrane-recruitment route that activate DVL3-dependent Wnt signaling in disease contexts.

    Evidence Met282 oxidation biochemistry and PNPO-DVL3 Co-IP in myeloma; WNT5B-FZD3-DVL3 Co-IP, DEP-domain deletion, RAC1/JNK assays in lung cancer

    PMID:39094673 PMID:39656865

    Open questions at the time
    • Structural consequence of Met282 oxidation not modeled
    • Single-lab findings each await independent confirmation
  9. 2025 High

    Resolved the phospho-regulated conformational logic of DVL3 and connected it to disease, showing how phosphorylation toggles DVL3 between FZD-bound and signaling-competent states.

    Evidence Phospho-switch mutant panel, BioID, in vitro phosphorylation, electrostatic/structural analysis; Robinow frameshift constructs with TOPFlash, ICC, phosphorylation assays; iPSC-NPC epistasis (PBX1 rescue); PCP BioID with zebrafish validation

    PMID:42127203 PMID:bio_10.1101_2025.01.15.633117 PMID:bio_10.1101_2025.03.12.642693 PMID:bio_10.1101_2025.08.02.668297

    Open questions at the time
    • Atomic structure of the DEP-disordered region switch not solved
    • How distinct C-terminal lengths in Robinow variants impair CK1 phosphorylation mechanistically unclear
    • Generality of PCP interactors (RAI14, EPHA2, PHACTR4) across tissues untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DVL3's distinct activities — phospho-switch-gated FZD release, nuclear transcriptional roles, the IGFIR-RAS adaptor function, and redox/degradation control — are coordinated within a single cell remains unresolved.
  • No unified model integrating cytoplasmic, membrane, and nuclear pools
  • Domain determinants partitioning canonical vs. non-canonical vs. non-Wnt functions not fully mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0140110 transcription regulator activity 1
Localization
GO:0005829 cytosol 3 GO:0005634 nucleus 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 1 R-HSA-74160 Gene expression (Transcription) 1
Partners
CCNL1CSNK1EDAB2FZD3IPMKMEX3APNPOWNT5B
Complex memberships
IGFIR-Shc-Grb2-SOS-DAB2 adaptor complexWNT5B-FZD3-DVL3 complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2026 Wnt stimulation triggers CK1-mediated multiphosphorylation of DVL3 that induces an intramolecular conformational switch between the DEP domain and the adjacent disordered region (phospho-switch), which is mutually exclusive with Frizzled receptor association. Charge accumulation proximal to the DEP domain is required (but not sufficient) for Wnt/β-catenin signaling. Proximity interactomics confirmed FZD receptors as prominent effectors of this phospho-switch. DVL3 phospho-switch mutant panel, proximity interactomics (BioID), in vitro phosphorylation assays, electrostatic/structural analysis Science advances High 42127203
2025 Pathogenic DVL3 frameshifting variants (novel basic C-terminus replacing ≥82 amino acids) fail to redistribute from cytoplasmic puncta to membrane upon WNT stimulation and fail to activate canonical WNT/β-catenin signaling (TOPFlash assay). The mutant C-terminal tail interferes with CSNK1E-induced phosphorylation of DVL3, providing a mechanism for impaired WNT response. Immunocytochemistry (localization), TOPFlash reporter assay (canonical WNT activation), transfection of WT vs. frameshift vs. truncated DVL1-3 constructs, in vitro phosphorylation assay bioRxivpreprint High bio_10.1101_2025.08.02.668297
2012 DVL3 translocates IPMK (inositol polyphosphate multikinase) to the cell membrane upon Wnt3a stimulation. This requires the PDZ domain and the C-terminal proline-rich tail of DVL3. Membrane translocation of IPMK is obligate for its function in Wnt signaling, and a deletion mutant of IPMK lacking the NH2-terminal variable region fails to translocate and cannot propagate canonical Wnt signaling. Co-immunoprecipitation, domain deletion mutants, cellular fractionation/imaging, Wnt3a stimulation assays Cellular signalling Medium 22940627
2024 WNT5B binding to FZD3 recruits DVL3 to the plasma membrane for phosphorylation in a WNT5B-dependent manner, and the DEP domain of DVL3 is required for this recruitment. DVL3 then activates RAC1 and downstream JNK signaling (non-canonical WNT/PCP pathway) in non-small cell lung cancer cells. Deletion of the DEP domain of DVL3 abrogated these effects. Co-immunoprecipitation (WNT5B-FZD3-DVL3 complex), domain deletion mutants (DEP domain), knockdown/overexpression, membrane fractionation, JNK/RAC1 activation assays Cellular signalling Medium 39094673
2016 ALFY (an autophagy scaffold protein) specifically removes aggregates of DVL3, but not DVL1 or DVL2, via autophagy-dependent degradation, thereby attenuating canonical Wnt signaling. Loss of ALFY function leads to DVL3 aggregate accumulation and increased Wnt signaling, contributing to brain size determination. Genetic linkage/exome sequencing (human microcephaly), Drosophila transgenic model, molecular biology (autophagy inhibition, aggregate analysis), isoform-specific knockdowns PLoS genetics High 27008544
2014 DVL3 is present in an adaptor complex that links IGFIR to RAS signaling, including Shc, Grb2, SOS, and the tumor suppressor DAB2. DVL3 blockade (genetic or pharmacologic) enhances MEK-ERK activation and sensitizes cells to IGFIR inhibition. Dual DVL3 and DAB2 blockade synergizes in activating ERKs, indicating a non-redundant role for DVL3 in the Shc-Grb2-SOS complex. Genetic screen, Co-immunoprecipitation (DVL3-Shc-Grb2-SOS-DAB2 complex), siRNA knockdown, in vivo xenograft, MEK-ERK activation assays Cancer research High 25168481
2011 Dvl-3 regulates both GSK-3 phosphorylation state and β-catenin levels downstream of the dopamine D2 receptor (D2DR) in rat brain. Altering Dvl-3 levels in SH-SY5Y cells changes Akt activity and the Wnt pathway similar to D2DR manipulation. Co-immunoprecipitation revealed association between GSK-3 and the D2DR complex that was altered by D2DR agonist/antagonist treatment. Co-immunoprecipitation (GSK-3/D2DR complex), Western blotting, in vitro manipulation of Dvl-3 in SH-SY5Y cells, pharmacological (raclopride, quinpirole) treatment The international journal of neuropsychopharmacology Medium 21777508
2019 DVL3 knockdown in rat Sertoli cells disrupts actin- and microtubule-based cytoskeleton organization, impairing tight junction-permeability barrier function. In vivo Dvl1/2/3 triple knockdown caused spermatid polarity defects, defective spermatid adhesion and transport, and disruptive spatial expression of actin- and MT-regulatory proteins. RNAi knockdown (individual Dvl1, Dvl2, Dvl3 and triple knockdown), physiological/biochemical assays (TJ-permeability barrier), morphological analysis, in vivo testis knockdown Cell death & disease Medium 30808893
2019 TLR4 activation by LPS induces Wnt3a and DVL3 expression in primary monocytes. DVL3 acts downstream of Wnt3a to promote β-catenin accumulation and restrain NF-κB activity, reducing pro-inflammatory cytokine production (IL-12, IL-6, TNFα). DVL3 siRNA silencing or Wnt3a inhibition significantly increases pro-inflammatory cytokine production and NF-κB P65 phosphorylation and DNA-binding activity. Gain- and loss-of-function (siRNA, ectopic expression of DVL3, GSK3β, β-catenin), ELISA, qRT-PCR, Western blot (signaling phosphorylation), murine endotoxin model (in vivo) Molecular immunology Medium 31884387
2018 DVL1 and DVL3 enter the nucleus and localize to at least two CYP19A1 (aromatase) promoters (pII and I.4) that drive overexpression in breast tumors, as well as a distal placental promoter (I.1). Loss-of-function of DVL-3 leads to differential changes in aromatase transcripts and estradiol (E2) production. Chromatin immunoprecipitation (ChIP) at CYP19A1 promoters, loss-of-function (DVL knockdown), aromatase transcript quantification, E2 production assay Oncotarget Medium 30479694
2022 DVL3 nuclear localization is required for its role in regulating proliferation in human myoblasts. DVL3 requires both the DIX and PDZ domains (unlike DVL1) for nuclear localization-dependent proliferation control. DVL1 and DVL3 regulate proliferation independently of markedly increased nuclear β-CATENIN translocation. Loss-of-function (knockdown), domain deletion/mutant constructs, nuclear localization imaging, proliferation assays in human myoblasts and rhabdomyosarcoma cells Scientific reports Medium 35589804
2022 MEX3A (RNA-binding protein) physically interacts with DVL3 and stabilizes β-catenin in endometrial carcinoma cells, activating Wnt/β-catenin downstream target genes and promoting EMT. This interaction was validated by co-immunoprecipitation. Co-immunoprecipitation (MEX3A-DVL3), immunofluorescence, siRNA knockdown and overexpression, in vitro and in vivo assays International journal of molecular sciences Medium 36614043
2024 PNPO (pyridoxine-5'-phosphate oxidase) oxidizes DVL3 at Met282, leading to abnormal activation of the Wnt/β-catenin pathway in multiple myeloma. Disrupting the PNPO-DVL3 interaction (by Eltrombopag) inhibits MM cell growth and reduces bone lesions. Chemical probe (celastrol) target identification, biochemical oxidation assay (DVL3 Met282 oxidation), Co-IP (PNPO-DVL3 interaction), mouse model, mutagenesis at critical PNPO sites Advanced science Medium 39656865
2013 AMPK activators (metformin) reduce DVL3 protein levels through two mechanisms: inhibition of mTOR-dependent DVL3 protein synthesis via AMPK/mTOR signaling, and promotion of ubiquitin/proteasomal degradation of DVL3. In vivo ubiquitination assay confirmed metformin-induced DVL3 ubiquitination. Enforced DVL3 expression elevated β-catenin and augmented cervical cancer cell growth, confirming DVL3 as a positive Wnt/β-catenin regulator. Western blot, in vivo ubiquitination assay, proteasomal inhibitors (MG132, AM114), AMPK inhibitor (Compound C), overexpression/knockdown, xenograft PloS one Medium 23301094
2025 DVL3 (along with CTNNB1 and PTEN) converges on PBX1 as a downstream target regulating neural progenitor cell (NPC) proliferation. In isogenic iPSC-derived NPCs with DVL3 ASD-related variants, PBX1a overexpression rescued increased NPC proliferation, establishing DVL3 upstream of PBX1 in NPC proliferation control. Isogenic iPSC-derived 2D NPCs, genetic epistasis (PBX1a overexpression rescue), proliferation assays bioRxivpreprint Medium bio_10.1101_2025.03.12.642693
2025 DVL3 proximity interactome (BioID) identified novel Wnt/PCP pathway components interacting with DVL3 in the cytoplasm. RAI14, EPHA2, and PHACTR4 were found as essential components connecting the PCP receptor complex to effector actomyosin. Proximity-dependent biotinylation (BioID) of DVL3 and other PCP components, zebrafish loss-of-function validation, subcellular compartment mapping bioRxivpreprint Medium bio_10.1101_2025.01.15.633117
1997 Human DVL3 (DVL-3) was cloned as a second human homolog of Drosophila Dishevelled. It encodes a 716 amino acid protein with 98% amino acid identity to mouse Dvl-3 and 49% to Drosophila Dsh. DVL-3 was mapped to chromosome 3q27. cDNA library screening, sequencing, chromosomal mapping, Northern blot expression analysis Biochemical and biophysical research communications High 9344861
2026 CCNL1 directly interacts with DVL3 (verified by Co-IP), and this interaction is negatively correlated with DVL3 levels. CCNL1 overexpression activates NF-κB signaling through its interaction with DVL3 and promotes the PI3K/AKT pathway in breast cancer cells. Co-immunoprecipitation (CCNL1-DVL3), Western blot, overexpression/knockdown, rescue assays Molecular carcinogenesis Low 41632921

Source papers

Stage 0 corpus · 41 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 AMPK activators suppress cervical cancer cell growth through inhibition of DVL3 mediated Wnt/β-catenin signaling activity. PloS one 75 23301094
2016 ALFY-Controlled DVL3 Autophagy Regulates Wnt Signaling, Determining Human Brain Size. PLoS genetics 73 27008544
2015 miR-204-5p promotes the adipogenic differentiation of human adipose-derived mesenchymal stem cells by modulating DVL3 expression and suppressing Wnt/β-catenin signaling. International journal of molecular medicine 62 25847080
2016 AMPK activators suppress breast cancer cell growth by inhibiting DVL3-facilitated Wnt/β-catenin signaling pathway activity. Molecular medicine reports 43 28035400
2018 DVL1 and DVL3 differentially localize to CYP19A1 promoters and regulate aromatase mRNA in breast cancer cells. Oncotarget 41 30479694
2011 The dopamine D2 receptor regulates Akt and GSK-3 via Dvl-3. The international journal of neuropsychopharmacology 39 21777508
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
2009 MSX1 induces the Wnt pathway antagonist genes DKK1, DKK2, DKK3, and SFRP1 in neuroblastoma cells, but does not block Wnt3 and Wnt5A signalling to DVL3. Cancer letters 37 19815336
2014 Dsh homolog DVL3 mediates resistance to IGFIR inhibition by regulating IGF-RAS signaling. Cancer research 28 25168481
2019 Planar cell polarity protein Dishevelled 3 (Dvl3) regulates ectoplasmic specialization (ES) dynamics in the testis through changes in cytoskeletal organization. Cell death & disease 27 30808893
2019 TLR4 induced Wnt3a-Dvl3 restrains the intensity of inflammation and protects against endotoxin-driven organ failure through GSK3β/β-catenin signaling. Molecular immunology 25 31884387
1997 cDNA cloning of a human dishevelled DVL-3 gene, mapping to 3q27, and expression in human breast and colon carcinomas. Biochemical and biophysical research communications 22 9344861
2021 LncRNA testis-specific transcript, Y-linked 15 (TTTY15) promotes proliferation, migration and invasion of colorectal cancer cells via regulating miR-29a-3p/DVL3 axis. Cancer biomarkers : section A of Disease markers 18 33016900
2020 Silencing DVL3 defeats MTX resistance and attenuates stemness via Notch Signaling Pathway in colorectal cancer. Pathology, research and practice 18 32414668
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
2018 Autosomal dominant Robinow syndrome associated with a novel DVL3 splice mutation. American journal of medical genetics. Part A 17 29575616
2024 Ginsenoside Rg3 suppresses vasculogenic mimicry by impairing DVL3-maintained stemness via PAAD cell-derived exosomal miR-204 in pancreatic adenocarcinoma. Phytomedicine : international journal of phytotherapy and phytopharmacology 15 38350242
2021 LncRNA BLACAT1 Promotes Proliferation, Migration and Invasion of Prostate Cancer Cells via Regulating miR-29a-3p/DVL3 Axis. Technology in cancer research & treatment 15 33641528
2022 DVL1 and DVL3 require nuclear localisation to regulate proliferation in human myoblasts. Scientific reports 14 35589804
2018 Role and mechanism of Dvl3 in the esophageal squamous cell carcinoma. European review for medical and pharmacological sciences 14 30536315
2022 E2F1-activated LINC01224 drives esophageal squamous cell carcinoma cell malignant behaviors via targeting miR-6884-5p/DVL3 axis and activating Wnt/β-catenin signaling pathway. Pathology, research and practice 13 35576835
2022 RNA-Binding Protein MEX3A Interacting with DVL3 Stabilizes Wnt/β-Catenin Signaling in Endometrial Carcinoma. International journal of molecular sciences 13 36614043
2024 PNPO-Mediated Oxidation of DVL3 Promotes Multiple Myeloma Malignancy and Osteoclastogenesis by Activating the Wnt/β-Catenin Pathway. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 11 39656865
2012 Dvl3 translocates IPMK to the cell membrane in response to Wnt. Cellular signalling 10 22940627
2024 WNT5B promotes the malignant phenotype of non-small cell lung cancer via the FZD3-DVL3-RAC1-PCP-JNK pathway. Cellular signalling 9 39094673
2022 Circ_0101802 Facilitates Colorectal Cancer Progression Depending on the Regulation of miR-665/DVL3 Signaling. Biochemical genetics 9 35314912
2018 Dvl3 polymorphism interacts with life events and pro-inflammatory cytokines to influence major depressive disorder susceptibility. Scientific reports 9 30242173
2017 Dishevelled segment polarity protein 3 (DVL3): a novel and easily applicable recurrence predictor in localised prostate adenocarcinoma. BJU international 8 28107606
2024 Dishevelled Segment Polarity Protein 3 (DVL3) Induced by Bacterial LPS Promotes the Proliferation and Migration of Prostate Cancer Cells through the TLR4 Pathway. Archivos espanoles de urologia 5 38583012
2022 The Gender-Specific Interaction of DVL3 and GSK3β Polymorphisms on Major Depressive Disorder Susceptibility in a Chinese Han Population: A Case-Control Study. Oxidative medicine and cellular longevity 5 35126809
2022 Exosomal Dvl3 promoted the aggressive phenotypic transformation of RA-FLS via wnt pathway. Autoimmunity 5 35499309
2021 Aberrant expression of SFRP1, SFRP3, DVL2 and DVL3 Wnt signaling pathway components in diffuse gastric carcinoma. Oncology letters 5 34691249
2023 Delivery of microRNA-423-5p by exosome from adipose-derived stem/stromal cells inhibits DVL3 to potentiate autologous fat graft survival through adipogenesis and inflammatory response. Human cell 4 38040867
2023 Presenilin-2 knock-In mice show severe depressive behavior via DVL3 downregulation. CNS neuroscience & therapeutics 3 37501340
2020 Retracted Article: Panax notoginseng saponins regulate VEGF to suppress esophageal squamous cell carcinoma progression via DVL3-mediated Wnt/β-catenin signaling. RSC advances 3 35497711
2020 Polymorphism and expression of the Dvl3 gene in the etiology of depressive disorder. Psychiatria polska 1 33038884
2026 CCNL1 Activates the NF-κB Pathway Through DVL3 Inhibition and PI3K/AKT Pathway Promotion in Breast Cancer. Molecular carcinogenesis 0 41632921
2026 A Wnt-induced conformational phospho-switch in DVL3 controls association with Frizzled receptors and Wnt/β-catenin signaling. Science advances 0 42127203
2025 E2F7 promotes ESCC progression and cisplatin resistance through transcriptional activation of DVL3 and the Wnt signaling pathway. World journal of surgical oncology 0 41327220
2022 [Effect of miR-204 targeted regulation of DVL3 gene in silica-induced mouse lung epithelial cells]. Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 0 35680573
2021 Retraction: Panax notoginseng saponins regulate VEGF to suppress esophageal squamous cell carcinoma progression via DVL3-mediated Wnt/β-catenin signaling. RSC advances 0 35427054

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