Affinage

DCBLD2

Discoidin, CUB and LCCL domain-containing protein 2 · UniProt Q96PD2

Length
775 aa
Mass
85.0 kDa
Annotated
2026-06-09
27 papers in source corpus 20 papers cited in narrative 21 extracted findings
Cross-family judge faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DCBLD2 (ESDN) is a type-I transmembrane neuropilin-like receptor that functions as a phosphorylation-dependent scaffold controlling the cell-surface residence and downstream signaling of multiple growth factor and cytokine receptors (PMID:11447234, PMID:24177422). Its intracellular YxxP motifs are phosphorylated by EGFR, Src-family kinases (notably Fyn), and Abl, and these phosphosites differentially recruit the SH2 adaptor CrkL; phosphorylation at Y565, Y621, Y715, and Y750 mediates CrkL binding, and antibody-induced receptor clustering is sufficient to trigger this phosphorylation (PMID:23770091, PMID:29025973). A distinct phosphosite, EGFR-driven phospho-Y750, lies within a TRAF6-binding motif and recruits TRAF6 to stimulate its E3 ubiquitin ligase activity and amplify AKT activation, driving EGFR-dependent tumorigenesis (PMID:25061874). In the vasculature, DCBLD2 associates with VEGFR-2 and regulates its complex with the negative regulators PTP1B, TC-PTP, and VE-cadherin to promote VEGF-induced endothelial proliferation, migration, and angiogenesis (PMID:24177422, PMID:41110167). A recurring mechanistic theme is control of receptor trafficking: DCBLD2 anchors PDGFR-β at the plasma membrane by competing with Caveolin-1 to block caveolae-dependent endocytosis (PMID:35929441), sustains insulin receptor surface levels through Rab11-dependent recycling (PMID:38872483), and limits clathrin-mediated TGF-β receptor endocytosis to suppress endothelial-to-mesenchymal transition (PMID:42178133). Consistent with an early-defined growth-suppressive role, DCBLD2 overexpression inhibits proliferation and tumor cell colony formation and invasion (PMID:11447234, PMID:18314483), yet it also negatively regulates insulin receptor signaling via the APS-c-Cbl and GRB10-NEDD4 adaptor-ligase pairs, such that Esdn deletion improves insulin sensitivity in vivo (PMID:26921437). A homozygous nonsense variant (p.W27*) in a patient impairs fibroblast proliferation and alters ROS and Ca2+ homeostasis, functionally characterizing loss of DCBLD2 (PMID:34145321).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2001 Medium

    Established DCBLD2/ESDN as a distinctive type-I transmembrane protein with CUB, coagulation factor V/VIII, and LCCL domains and an unusually long signal sequence, and gave the first functional clue that it restrains proliferation.

    Evidence Signal-sequence trap cloning, domain analysis, and BrdU uptake after overexpression in 293T cells

    PMID:11447234

    Open questions at the time
    • No binding partners or signaling mechanism identified
    • Antiproliferative effect based on overexpression only
  2. 2007 Medium

    Connected DCBLD2 to vascular biology by showing it regulates proliferation of vascular smooth muscle cells bidirectionally with gene dose.

    Evidence ESDN overexpression and siRNA knockdown in primary VSMCs with growth-curve readout

    PMID:17697260

    Open questions at the time
    • Molecular mechanism of growth control unresolved
    • No receptor partner defined
  3. 2007 Medium

    Identified DCBLD2 as a tyrosine-phosphorylation substrate of EGFR signaling, placing it downstream of growth-factor receptor activation.

    Evidence cICAT phosphoproteomics in EGF-treated A431 cells with EGFR-inhibitor (Iressa) validation

    PMID:17570516

    Open questions at the time
    • Specific phosphosites not mapped
    • Functional consequence of phosphorylation not shown
  4. 2010 Medium

    Dissected the long signal sequence into NtraC subdomains, showing the C-domain alone drives ER targeting and freeing the N-domain for additional functions.

    Evidence Deletion/chimeric constructs with ER-targeting assays

    PMID:21183991

    Open questions at the time
    • Function of the dispensable N-domain not defined
    • No partner identified for the retained segment at this stage
  5. 2013 High

    Defined the phosphorylation logic of the cytoplasmic tail, showing SFKs phosphorylate YxxP tyrosines that recruit the CrkL SH2 domain and that receptor clustering activates this circuit.

    Evidence Site-directed mutagenesis of seven tyrosines, quantitative MS, SH2 pulldowns, SFK inhibition, and antibody clustering

    PMID:23770091

    Open questions at the time
    • Downstream output of CrkL recruitment not traced
    • Physiological clustering ligand unknown
  6. 2013 High

    Established DCBLD2 as a positive regulator of VEGFR-2 signaling in endothelium by genetic loss and partner mapping, distinguishing it from its growth-suppressive role elsewhere.

    Evidence Global, EC-specific, and zebrafish loss-of-function; reciprocal Co-IP with VEGFR-2, PTP1B, TC-PTP, VE-cadherin; in vivo VEGF signaling assays

    PMID:24177422

    Open questions at the time
    • Structural basis of VEGFR-2 association not resolved
    • Mechanism of displacing PTP1B/TC-PTP not detailed
  7. 2014 High

    Resolved a specific oncogenic phosphosite pathway: EGFR-phosphorylated Y750 recruits TRAF6 to boost its ligase activity and AKT signaling, driving tumorigenesis.

    Evidence Phospho-specific antibodies, Y750 mutagenesis, TRAF6 Co-IP and E3 ligase assays, AKT readouts, and xenograft models

    PMID:25061874

    Open questions at the time
    • TRAF6 ubiquitination substrate in this context not defined
    • Link between Y750 and the CrkL-binding sites not integrated
  8. 2016 High

    Showed DCBLD2 negatively regulates insulin receptor signaling through adaptor-E3 ligase pairs, giving it a systemic metabolic role.

    Evidence Esdn knockout mice with glucose/insulin tolerance tests, InsR Co-IP, AKT/MAPK blots, and VSMC assays

    PMID:26921437

    Open questions at the time
    • How DCBLD2 modulates APS-c-Cbl and GRB10-NEDD4 binding mechanistically unclear
    • Reconciliation with later positive InsR-recycling role unresolved
  9. 2017 High

    Refined the kinase-phosphosite code by showing Fyn and Abl differentially phosphorylate individual YxxP sites to tune CrkL recruitment.

    Evidence Site-specific quantitative phosphoproteomics, kinase overexpression, CrkL-SH2 pulldowns, and kinase inhibition

    PMID:29025973

    Open questions at the time
    • Cellular contexts engaging Fyn versus Abl not defined
    • Downstream signaling differences between sites not measured
  10. 2021 Medium

    Expanded the partner repertoire and disease links: DCBLD2 binds ITGB1 (focal adhesion), stabilizes β-catenin via GSK3β to drive lung adenocarcinoma metastasis, suppresses endothelial E-selectin to limit melanoma extravasation, and a nonsense variant impairs fibroblast proliferation.

    Evidence TAP-MS/Co-IP (ITGB1); siRNA with GSK3β/β-catenin readouts and in vivo metastasis; Esdn-null melanoma model with E-selectin quantification; whole-exome sequencing and patient fibroblast assays

    PMID:33808696 PMID:33862151 PMID:34095137 PMID:34145321

    Open questions at the time
    • STAT3 link to E-selectin not directly demonstrated
    • No rescue for the p.W27* patient variant
    • Mechanism linking DCBLD2 to GSK3β phosphorylation unresolved
  11. 2022 High

    Defined a trafficking mechanism: DCBLD2 retains PDGFR-β at the membrane by competing with Caveolin-1 to block caveolae-dependent internalization and lysosomal degradation.

    Evidence Germline and conditional Dcbld2 knockout mice, PDGFR-β/Cav-1/DCBLD2 Co-IP, surface biotinylation, fractionation, and imaging

    PMID:35929441

    Open questions at the time
    • Whether the same competition applies to other receptors not tested here
    • Structural basis of Cav-1 competition unknown
  12. 2023 Medium

    Identified CD146 as a stabilizer of DCBLD2 protein that activates PI3K/AKT in phyllodes tumor cells, adding upstream regulation of DCBLD2 abundance.

    Evidence Reciprocal Co-IP, pulldown, omics, and proliferation/invasion assays

    PMID:37856423

    Open questions at the time
    • Degradation pathway prevented by CD146 not defined
    • Single tumor context
  13. 2024 High

    Extended the trafficking model to insulin receptor recycling, showing DCBLD2 sustains InsR surface levels and InsR/PI3K/Akt signaling via Rab11-dependent recycling, with vascular consequences in diabetes.

    Evidence Endothelium-specific and global Dcbld2 knockout mice, streptozotocin diabetes model, InsR Co-IP, fractionation, glycolytic and signaling assays

    PMID:38872483

    Open questions at the time
    • Apparent contrast with earlier negative InsR regulation not mechanistically reconciled
    • Direct role in Rab11 recruitment not shown
  14. 2024 Medium

    Provided a molecular basis for VEGFR-2 association by showing the uncleaved signal sequence's hydrophobic traC segment binds VEGFR-2, and a derived peptide promotes angiogenesis.

    Evidence Co-IP of DCBLD2 domain constructs with VEGFR2, synthetic peptide signaling assays, matrigel/corneal angiogenesis, and hindlimb ischemia (preprint)

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Structural detail of the traC–VEGFR2 interface limited
  15. 2026 Medium

    Generalized the endocytosis-blocking mechanism to TGF-βR, where DCBLD2 binds TGF-βR and clathrin to limit clathrin-mediated internalization, suppress EndMT, and protect against calcific aortic valve disease.

    Evidence DCBLD2 knockout mice, DCBLD2–TGF-βR/clathrin Co-IP, TGF-β pathway blots, Pitstop 2 rescue, and migration assays

    PMID:42178133

    Open questions at the time
    • Direct competition with the clathrin machinery not quantified
    • Single lab
  16. 2026 Medium

    Identified miR-34c-3p as a direct upstream repressor of DCBLD2 mRNA controlling osteogenic differentiation through PI3K/AKT.

    Evidence DCBLD2 overexpression/knockdown in BMSCs, ALP/alizarin red staining, PI3K activator rescue, AGO2-RIP, and dual-luciferase reporter

    PMID:41721921

    Open questions at the time
    • In vivo relevance to bone not tested
    • Receptor partner mediating PI3K/AKT in BMSCs not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DCBLD2's growth-suppressive versus signaling-amplifying roles and its opposing effects on insulin receptor activity are integrated into a single regulatory logic remains unresolved.
  • No unifying model reconciling negative InsR regulation (2016) with InsR-recycling support (2024)
  • No structural model of the full receptor or its receptor-binding interfaces
  • Endogenous ligand/clustering trigger for the cytoplasmic phosphorylation circuit unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0060090 molecular adaptor activity 3
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 3 R-HSA-5653656 Vesicle-mediated transport 3
Partners
CAV1CRKLEGFRINSRITGB1PDGFRBTRAF6VEGFR2

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 ESDN/DCBLD2 is a type-I transmembrane protein containing a CUB domain, a coagulation factor V/VIII homology domain, and an LCCL domain, and harbors the longest cleavable secretory signal sequence among eukaryotes. Overexpression of ESDN in 293T cells suppressed BrdU uptake, indicating a role in inhibiting cell proliferation. Signal sequence trap cloning, domain analysis, overexpression in 293T cells with BrdU uptake assay The Journal of biological chemistry Medium 11447234
2007 DCBLD2 (ESDN) is upregulated in proliferating vascular smooth muscle cells (VSMCs); ESDN overexpression in VSMCs decreased growth, while ESDN knockdown increased VSMC proliferation, establishing ESDN as a regulator of VSMC proliferation. VSMC culture with ESDN overexpression and siRNA knockdown; growth curve analysis American journal of transplantation Medium 17697260
2007 DCBLD2 is a novel tyrosine phosphorylation target of EGF/EGFR signaling, identified and validated by phosphoproteomics; phosphorylation is blocked by the EGFR inhibitor Iressa. cICAT-based LC-MS/MS phosphoproteomics from EGF-treated A431 cells, validated by western blot with EGFR inhibitor Proteomics Medium 17570516
2008 Ectopic expression of DCBLD2 in gastric cancer cell lines inhibited colony formation (anchorage-dependent and -independent) and inhibited invasion through collagen matrix, demonstrating a suppressive role in gastric cancer cell proliferation and invasion. Ectopic expression in gastric cancer cell lines; colony formation assay, collagen matrix invasion assay Molecular cancer research : MCR Medium 18314483
2010 The long signal peptide of DCBLD2 can be dissected into functional N and C subdomains per the NtraC model: the C-domain is sufficient and essential for ER targeting, whereas the N-domain is dispensable and thus available for additional functions. Deletion/chimeric construct expression; ER targeting assay Molecular bioSystems Medium 21183991
2013 DCBLD2 (ESDN) intracellular tyrosines in YxxP motifs are phosphorylated by Src family kinases (SFKs); phosphorylation at Y565, Y621, Y750, and Y715 (non-YxxP) recruits the SH2 domain of the signaling adaptor CrkL. Antibody-mediated ESDN clustering induces tyrosine phosphorylation and CrkL-SH2 binding. Mutagenesis of seven intracellular tyrosines; quantitative mass spectrometry; SH2 domain pulldown; pharmacological SFK inhibition; antibody clustering assay FEBS letters High 23770091
2013 ESDN/DCBLD2 promotes VEGF-induced endothelial cell proliferation and migration; it associates with VEGFR-2 and regulates VEGFR-2 complex formation with the negative regulators PTP1B, TC-PTP, and VE-cadherin. Loss of ESDN in EC-specific knockout mice blunted VEGF responses and VEGFR-2 signaling in vivo. Global and EC-specific Esdn knockout mice; zebrafish dcbld2 knockdown; Co-IP of ESDN with VEGFR-2, PTP1B, TC-PTP, and VE-cadherin; VEGFR-2 signaling assays The Journal of clinical investigation High 24177422
2014 EGFR phosphorylates DCBLD2 at tyrosine 750 (Y750), which lies within a TRAF6-binding motif. Phospho-Y750 recruits TRAF6, leading to increased TRAF6 E3 ubiquitin ligase activity and subsequent AKT activation, thereby promoting EGFR-driven tumorigenesis. Phospho-specific antibodies; Co-IP of DCBLD2 Y750 with TRAF6; TRAF6 E3 ubiquitin ligase activity assay; AKT activation assays; tumor xenograft models; Y750 mutagenesis The Journal of clinical investigation High 25061874
2016 ESDN/DCBLD2 inhibits insulin receptor signaling by interacting with the insulin receptor and altering its interaction with the regulatory adaptor-E3 ubiquitin ligase pairs APS-c-Cbl and GRB10-NEDD4. Esdn gene deletion enhances insulin-induced AKT and MAPK activation, VSMC proliferation/migration, and improves insulin sensitivity and glucose homeostasis in vivo. Esdn knockout mice; in vivo glucose/insulin tolerance tests; Co-IP of ESDN with insulin receptor; western blot for AKT/MAPK phosphorylation; VSMC proliferation/migration assays American journal of physiology. Heart and circulatory physiology High 26921437
2017 DCBLD2 intracellular YxxP motifs are phosphorylated by Src family kinases (SFKs; specifically Fyn) and Abl kinase, which differentially promote CRKL-SH2 domain binding to DCBLD2. Site-specific quantitative phosphoproteomics mapped the SFK vs. Abl preferences for individual YxxP sites on DCBLD2. HPLC-coupled tandem mass spectrometry; kinase overexpression; CRKL-SH2 pulldown; pharmacological kinase inhibition The Biochemical journal High 29025973
2021 DCBLD2 stabilizes β-catenin by phosphorylating GSK3β; accumulated β-catenin is transported to the nucleus to promote EMT-related transcription factor expression, mediating cisplatin-induced metastasis in lung adenocarcinoma. siRNA knockdown, western blot for GSK3β phosphorylation and β-catenin nuclear translocation, in vitro migration/invasion assays, in vivo metastasis model with nanoparticle-delivered siRNA Cancers Medium 33808696
2021 A homozygous nonsense variant (p.W27*) in DCBLD2 in a patient results in reduced cell proliferation, impaired cell cycle progression, and altered intracellular ROS and Ca2+ levels in patient-derived skin fibroblasts, functionally characterizing this loss-of-function variant. Whole-exome sequencing; in vitro functional studies on patient skin fibroblasts (proliferation, cell cycle, ROS, Ca2+ assays) Scientific reports Medium 34145321
2021 DCBLD2 binds ITGB1 (integrin β1, a key focal adhesion pathway component) as identified by TAP-MS and confirmed by Co-IP, implicating DCBLD2 in the focal adhesion pathway in colorectal cancer cells. TAP-MS affinity purification followed by Co-IP validation Frontiers in cell and developmental biology Medium 34095137
2021 In endothelial cells, ESDN/DCBLD2 loss leads to increased E-selectin transcript and protein levels, enhanced melanoma cell adhesion and extravasation, and increased metastasis in Esdn-null mice. ESDN suppresses E-selectin transcription, potentially through STAT3. Esdn-null mouse melanoma injection model; endothelial cell adhesion assay; E-selectin mRNA/protein quantification; cimetidine (E-selectin inhibitor) rescue experiment Cancer letters Medium 33862151
2022 DCBLD2 inhibits caveolae-dependent endocytosis of PDGFR-β in VSMCs by anchoring PDGFR-β on the cell membrane via competition with Caveolin-1 (Cav-1). DCBLD2 deletion increases PDGFR-β–Cav-1 binding and accelerates PDGF-induced PDGFR-β internalization to lysosomes. VSMC-conditional and germline Dcbld2 knockout mice; Co-IP of PDGFR-β with Cav-1 and DCBLD2; biotin surface labeling; membrane/cytosol fractionation; double immunofluorescence FASEB journal High 35929441
2023 CD146 protein physically interacts with DCBLD2 and prevents its degradation, thereby stabilizing DCBLD2 and activating downstream PI3K/AKT signaling in breast phyllodes tumor cells. Co-immunoprecipitation, pull-down assay, transcriptome and proteomic analysis, functional proliferation/invasion assays Cancer communications (London, England) Medium 37856423
2024 DCBLD2 deletion in endothelial cells inhibits insulin receptor recycling in a Rab11-dependent manner, reduces membrane InsR levels, and attenuates InsR/PI3K/Akt signaling, exacerbating endothelial dysfunction and vascular remodeling in diabetic mice. Endothelium-specific and global Dcbld2 knockout mice; streptozotocin-induced diabetes model; Co-IP for InsR interactions; membrane/cytoplasm fractionation; glycolytic rate assay; western blot The FEBS journal High 38872483
2025 DCBLD2 and VEGFA act synergistically in choroidal endothelial cells to enhance proliferation, migration, and angiogenic tube formation; DCBLD2 potentiates VEGFA-driven effects by increasing VEGFR2 phosphorylation and activating downstream AKT and ERK1/2 signaling cascades. Functional validation in choroidal endothelial cells (proliferation, migration, tube formation assays); VEGFR2 phosphorylation western blot; AKT/ERK1/2 activation assays Journal of proteome research Medium 41110167
2026 DCBLD2 loss in endothelial cells enhances TGF-β signaling by increasing clathrin-mediated endocytosis of TGF-β receptor (TGF-βR); DCBLD2 interacts with TGF-βR and clathrin, and its loss promotes EndMT. DCBLD2 knockout mice show higher prevalence of calcific aortic valve disease. DCBLD2 knockout mice; immunoprecipitation of DCBLD2 with TGF-βR and clathrin; western blot for TGF-β pathway phosphorylation; Pitstop 2 clathrin inhibitor rescue; immunofluorescence; endothelial migration assay Journal of molecular and cellular cardiology Medium 42178133
2026 DCBLD2 overexpression inhibits osteogenic differentiation of BMSCs and suppresses PI3K/AKT pathway activation; miR-34c-3p directly binds DCBLD2 mRNA (confirmed by AGO2-RIP and dual-luciferase assay) to suppress its expression and thereby promote osteogenic differentiation. Overexpression and knockdown of DCBLD2 in BMSCs; ALP and alizarin red staining; PI3K activator rescue; AGO2-RIP; dual-luciferase reporter assay Journal of molecular histology Medium 41721921
2024 The signal sequence (SS) of DCBLD2 is not cleaved in the mature protein and directly interacts with VEGFR2 via its hydrophobic 'traC' segment (specifically the L5VL5/L10 sequence). The SS promotes VEGF-induced signaling, and a synthetic traC-derived peptide (L10) enhances VEGFR2 signaling in vitro and promotes angiogenesis and blood flow recovery in vivo. Co-immunoprecipitation of DCBLD2 domain constructs with VEGFR2 in HEK293T and endothelial cells; synthetic peptide signaling assays; matrigel plug and corneal micropocket angiogenesis assays; hindlimb ischemia model bioRxivpreprint Medium

Source papers

Stage 0 corpus · 27 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 EGFR phosphorylation of DCBLD2 recruits TRAF6 and stimulates AKT-promoted tumorigenesis. The Journal of clinical investigation 75 25061874
2001 ESDN, a novel neuropilin-like membrane protein cloned from vascular cells with the longest secretory signal sequence among eukaryotes, is up-regulated after vascular injury. The Journal of biological chemistry 61 11447234
2013 Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis. The Journal of clinical investigation 57 24177422
2008 Epigenetic down-regulation and suppressive role of DCBLD2 in gastric cancer cell proliferation and invasion. Molecular cancer research : MCR 46 18314483
2007 Phosphoproteomics identified Endofin, DCBLD2, and KIAA0582 as novel tyrosine phosphorylation targets of EGF signaling and Iressa in human cancer cells. Proteomics 44 17570516
2021 DCBLD2 Affects the Development of Colorectal Cancer via EMT and Angiogenesis and Modulates 5-FU Drug Resistance. Frontiers in cell and developmental biology 29 34095137
2007 ESDN is a marker of vascular remodeling and regulator of cell proliferation in graft arteriosclerosis. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 22 17697260
2017 Dynamic multi-site phosphorylation by Fyn and Abl drives the interaction between CRKL and the novel scaffolding receptors DCBLD1 and DCBLD2. The Biochemical journal 20 29025973
2021 DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma. Cancers 18 33808696
2016 The neuropilin-like protein ESDN regulates insulin signaling and sensitivity. American journal of physiology. Heart and circulatory physiology 18 26921437
2022 DCBLD2 regulates vascular hyperplasia by modulating the platelet derived growth factor receptor-β endocytosis through Caveolin-1 in vascular smooth muscle cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 17 35929441
2023 CD146 promotes malignant progression of breast phyllodes tumor through suppressing DCBLD2 degradation and activating the AKT pathway. Cancer communications (London, England) 16 37856423
2013 Tyrosine phosphorylation of the orphan receptor ESDN/DCBLD2 serves as a scaffold for the signaling adaptor CrkL. FEBS letters 14 23770091
2022 miR-451a suppresses papillary thyroid cancer cell proliferation and invasion and facilitates apoptosis through targeting DCBLD2 and AKT1. Molecular and cellular probes 11 36252912
2021 A homozygous nonsense mutation in DCBLD2 is a candidate cause of developmental delay, dysmorphic features and restrictive cardiomyopathy. Scientific reports 11 34145321
2012 DCBLD2 gene variations correlate with nasal polyposis in Korean asthma patients. Lung 9 22261696
2021 ESDN inhibits melanoma progression by blocking E-selectin expression in endothelial cells via STAT3. Cancer letters 7 33862151
2024 LncRNA MIR100HG affects the proliferation and metastasis of lung cancer cells through mediating the microRNA-5590-3p/DCBLD2 axis. Immunity, inflammation and disease 6 38602284
2012 Potential association of DCBLD2 polymorphisms with fall rates of FEV(1) by aspirin provocation in Korean asthmatics. Journal of Korean medical science 6 22468095
2024 DCBLD2 deletion increases hyperglycemia and induces vascular remodeling by inhibiting insulin receptor recycling in endothelial cells. The FEBS journal 5 38872483
2010 Long signal peptides of RGMa and DCBLD2 are dissectible into subdomains according to the NtraC model. Molecular bioSystems 4 21183991
2023 Engineering siRNA-loaded and RGDfC-targeted selenium nanoparticles for highly efficient silencing of DCBLD2 gene for colorectal cancer treatment. Discover nano 3 37477789
2026 miR-34c-3p promotes osteogenic differentiation of BMSCs by inhibiting DCBLD2 activation of the PI3K/AKT signaling pathway. Journal of molecular histology 0 41721921
2026 Integrative analysis identifies DCBLD2 and immune-related biomarkers for major depressive disorder: evidence from human peripheral blood, post-mortem brain, and rat models. Frontiers in human neuroscience 0 42148317
2026 The mechanistic of DCBLD2 in inhibiting TGF-β induced endothelial-mesenchymal transition in calcific aortic valve disease. Journal of molecular and cellular cardiology 0 42178133
2025 Integrating OLINK Proteomics and Single-Cell Analysis Reveals that DCBLD2 Potentiates VEGFA-Driven Angiogenesis in Retinal Detachment with Choroidal Detachment. Journal of proteome research 0 41110167
2025 Integrated Multiomics Unravels Hedgehog (HH) Signaling Characteristics in Pancreatic Cancer (PC) and DCBLD2 Regulates HH Signaling to Drive PC Progression. Human mutation 0 41427028

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