Affinage

Showing POPDC1 — BVES is a alias.

POPDC1

Popeye domain-containing protein 1 · UniProt Q8NE79

Length
360 aa
Mass
41.5 kDa
Annotated
2026-06-10
61 papers in source corpus 22 papers cited in narrative 22 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

POPDC1/BVES is a three-pass transmembrane protein with an extracellular, glycosylated N-terminus and a cytoplasmic C-terminus that functions as a membrane-localized scaffold coordinating cell adhesion, junctional integrity, vesicular recycling, and cAMP-dependent signaling (PMID:11493530, PMID:12815060). It first localizes to lateral epithelial membranes at sites of cell-cell contact and confers adhesive behavior on non-adherent cells, acting through an intracellular homodimerization domain (K272/K273) required for adhesion and junction assembly (PMID:11493530, PMID:18493308). Its cytoplasmic tail directly binds ZO-1 to maintain tight junction integrity and transepithelial resistance, places POPDC1 upstream of the PAR/aPKC complex, and restrains RhoA, Rac1, and Cdc42 signaling—both via direct interaction with the Rho-family GEF GEFT and through GEF-H1/ZONAB regulation—thereby suppressing epithelial-to-mesenchymal transition (PMID:16188940, PMID:18541910, PMID:21283798, PMID:23019331, PMID:21911938). Through direct binding to the SNARE protein VAMP3 and to NDRG4, POPDC1 controls recycling-endosome fusion and trafficking of transferrin, β1-integrin, and fibronectin, supporting directional cell movement (PMID:20057356, PMID:24048452). In striated muscle and heart, POPDC1 binds cAMP via its Popeye domain and functions as a negative-feedback regulator of adenylyl cyclase 9 (ADCY9): it scaffolds an AC9–TREK-1 potassium channel complex at the sarcolemma whose composition is tuned by β-adrenergic signaling, and it restrains AC9–cAMP–PKA signaling to limit FoxO-driven proteasomal degradation and autophagy, controlling cardiac pacemaking and muscle mass (PMID:36254885, PMID:36997581). POPDC1 associates with caveolin-3 in cardiac caveolae to support ischemic preconditioning and Ca2+ handling (PMID:24066022). The loss-of-function S201F variant reduces cAMP binding and impairs membrane trafficking of POPDC1 and POPDC2, causing limb-girdle muscular dystrophy with cardiac arrhythmia (PMID:26642364).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2001 High

    Establishing what kind of molecule BVES is: it was identified as a novel membrane protein that confers cell adhesion and localizes to sites of cell-cell contact, defining it as a cell adhesion molecule.

    Evidence L-cell transfection adhesion assay, antibody inhibition of epicardial migration, immunofluorescence localization

    PMID:11493530

    Open questions at the time
    • No binding partner identified for the adhesive activity
    • Mechanism of contact accumulation unresolved
  2. 2003 High

    Resolving the membrane topology was needed to interpret which terminus engages cytoplasmic partners; biochemistry established an extracellular glycosylated N-terminus, three TM domains, and a cytoplasmic C-terminus.

    Evidence Glycosylation assays, glycosylation-site insertion, topology-reversal constructs, permeabilization immunoreactivity

    PMID:12815060

    Open questions at the time
    • No structural model of the cytoplasmic domain
    • Functional roles of N- vs C-terminus not yet assigned
  3. 2005 High

    Identifying the first direct binding partner connected BVES to junctional biology: its C-terminus binds ZO-1 and is required to maintain tight junction integrity.

    Evidence GST pull-down, TJ marker localization, siRNA knockdown with transepithelial resistance

    PMID:16188940

    Open questions at the time
    • Binding interface on ZO-1 not mapped
    • Whether ZO-1 binding is direct in vivo not addressed
  4. 2008 High

    Two studies defined how BVES restrains Rho-family signaling and self-associates: it binds the GEF GEFT to suppress Rac1/Cdc42, and an intracellular homodimerization domain (K272/K273) is essential for adhesion and junction assembly.

    Evidence Co-IP/pulldown, Rho GTPase activity assays, GST pull-down, SPOTS, site-directed mutagenesis, transepithelial resistance

    PMID:18493308 PMID:18541910

    Open questions at the time
    • RhoA-specific regulation mechanism distinct from GEFT not resolved
    • Stoichiometry of homodimer unknown
  5. 2010 High

    Linking BVES to membrane trafficking, it was shown to bind the SNARE VAMP3 and control recycling of transferrin and β1-integrin, with in vivo gastrulation consequences.

    Evidence Co-IP, transferrin/integrin recycling assays, Xenopus morpholino knockdown, kymography

    PMID:20057356

    Open questions at the time
    • How BVES regulates VAMP3 fusion machinery mechanistically unclear
    • Cargo selectivity not fully defined
  6. 2011 High

    BVES was placed as a suppressor of EMT and RhoA/ZONAB signaling, connecting its junctional role to tumor-relevant phenotypes.

    Evidence Re-expression and dominant-negative constructs in cancer cells, xenograft, FRET RhoA assay, ZONAB luciferase reporter

    PMID:21283798 PMID:21911938

    Open questions at the time
    • Direct mechanism linking ZO-1 loss to GEF-H1/RhoA activation incomplete
    • ZONAB regulation is correlative
  7. 2013 High

    Two studies extended trafficking and membrane-microdomain roles: BVES binds NDRG4 to drive recycling-endosome fusion for directional migration, and associates with caveolin-3 to support cardiac caveolae and ischemic preconditioning.

    Evidence Protein interaction assays, TIRF of endosome fusion, fibronectin recycling, Co-IP with caveolin-3, density gradients, EM, knockout ischemia/reperfusion model

    PMID:24048452 PMID:24066022

    Open questions at the time
    • Whether NDRG4 and caveolin-3 functions are mechanistically linked unknown
    • Caveolae loss mechanism downstream of POPDC1 not defined
  8. 2015 High

    The S201F disease variant established cAMP binding as functionally critical: it reduces cAMP affinity and impairs membrane trafficking of POPDC1 and POPDC2, causing muscular dystrophy with arrhythmia.

    Evidence cAMP-binding affinity assay, patient muscle immunohistochemistry, HL-1 electrophysiology, zebrafish knockin

    PMID:26642364

    Open questions at the time
    • How cAMP binding regulates downstream effectors not yet mechanistically defined here
    • POPDC1-POPDC2 heterodimer trafficking mechanism unresolved
  9. 2022 High

    Defining a cardiac signaling module, POPDC1 was shown to scaffold an AC9-TREK-1 potassium channel complex whose TREK-1 association is tuned by β-adrenergic input, providing a molecular basis for pacemaking control.

    Evidence Reciprocal Co-IP, co-purification, TREK-1 electrophysiology, Adcy9 knockout mice with heart rate recording, βAR stimulation

    PMID:36254885

    Open questions at the time
    • How POPDC1 cAMP binding couples to TREK-1 gating not fully resolved
    • Whether AC9-POPDC1 scaffolding generalizes beyond heart untested here
  10. 2023 High

    The cAMP-effector logic in skeletal muscle was clarified: POPDC1 directly binds and negatively regulates ADCY9, restraining PKA-FoxO-driven proteolysis and autophagy to maintain muscle mass.

    Evidence Bves knockout mice, BVES-ADCY9 Co-IP, cAMP/PKA assays, AAV rescue, FoxO and autophagy readouts

    PMID:36997581

    Open questions at the time
    • Structural basis of ADCY9 inhibition unknown
    • Role of cAMP binding by POPDC1 in this regulation not directly tested here
  11. 2022 Medium

    Additional partners and tissue roles broadened the scaffolding picture: POPDC1 engages XIRP1/actin at intercalated discs, PR61α-PP2A to control c-Myc/Wnt, Dusp1-MAPK in vascular smooth muscle, and restrains hippocampal LTP via cAMP-PKA.

    Evidence Proteomic pull-down and Co-IP (XIRP1), yeast two-hybrid and AOM/DSS model (PR61α), RNA-seq and aortic graft model (Dusp1), knockout slice electrophysiology (LTP)

    PMID:28389570 PMID:33261556 PMID:34937090 PMID:36037759

    Open questions at the time
    • Several interactions rest on single-lab evidence
    • Mechanistic connections among these tissue-specific roles not integrated
  12. 2021 Medium

    POPDC1 was linked to ER-resident muscle biology through interaction with ANO5, with both required for myoblast differentiation.

    Evidence BioID2 proximity labeling, mass spectrometry, Co-IP, domain mapping, CRISPR knockout differentiation assay

    PMID:34963485

    Open questions at the time
    • Functional consequence of ER co-localization unclear
    • Single-lab interaction without reciprocal in vivo validation
  13. 2024 Medium

    POPDC1 dysfunction was tied to AV node–specific conduction defects and sympathetic-dependent arrhythmogenesis.

    Evidence Action potential and calcium imaging in zebrafish mutants/knockouts, isoproterenol stimulation

    PMID:38540339

    Open questions at the time
    • Which POPDC1 effector complex drives AV node phenotype not pinpointed
    • Single-lab zebrafish data

Open questions

Synthesis pass · forward-looking unresolved questions
  • How cAMP binding to the Popeye domain mechanistically toggles POPDC1's multiple effector interactions (AC9, TREK-1, trafficking partners) into a unified regulatory output remains unresolved.
  • No high-resolution structure of POPDC1 bound to effectors
  • Integration of junctional, trafficking, and cAMP-signaling roles in one tissue untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 5 GO:0098772 molecular function regulator activity 2 GO:0008289 lipid binding 1 GO:0098631 cell adhesion mediator activity 1
Localization
GO:0005886 plasma membrane 4 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1500931 Cell-Cell communication 2 R-HSA-397014 Muscle contraction 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
ADCY9ANO5CAV3GEFTNDRG4VAMP3XIRP1ZO-1
Complex memberships
AC9-TREK-1-POPDC1 sarcolemmal complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 BVES/POPDC1 is a membrane protein with three transmembrane helices, an extracellular N-terminus and an intracellular C-terminus, confined to the lateral membrane compartment of epithelial cells. It accumulates at points of cell-cell contact before E-cadherin appearance, and transfection into non-adherent L-cells confers adhesive behavior, establishing it as a novel cell adhesion molecule. Transfection into L-cells (adhesion assay), antibody inhibition of epicardial migration, subcellular localization by immunofluorescence Development (Cambridge, England) High 11493530
2003 The membrane topology of BVES/Pop1A consists of an extracellular N-terminus (glycosylated), three transmembrane domains, and a cytoplasmic C-terminus. This was established by glycosylation assays, topology-reversal constructs, and differential immunoreactivity with/without detergent permeabilization. Glycosylation assays, glycosylation-site insertion constructs, co-expression topology experiments, selective immunoreactivity assay on intact vs. permeabilized cells The Journal of biological chemistry High 12815060
2005 BVES localizes with tight junction markers ZO-1 and occludin in polarized epithelial cells. GST pull-down demonstrates a direct interaction between ZO-1 and the intracellular C-terminal tail of BVES. Knockdown of BVES causes loss of transepithelial resistance and junctional protein membrane localization, demonstrating BVES modulates tight junction integrity. GST pull-down, immunolocalization with TJ markers, Ca2+-chelation/TPA challenge, siRNA knockdown with transepithelial resistance measurement Journal of cell science High 16188940
2008 BVES directly interacts with GEFT (a GEF for Rho-family GTPases), co-localizing in adult skeletal muscle. Exogenous BVES expression reduces Rac1 and Cdc42 activity levels without affecting RhoA activity, and produces corresponding changes in cell locomotion speed and cell roundness. Co-immunoprecipitation/pulldown interaction assay, co-localization, Rho GTPase activity assays, cell motility and morphology analysis Proceedings of the National Academy of Sciences of the United States of America High 18541910
2008 BVES interacts with itself through a specific intracellular homodimerization domain (amino acids 268-274, critical residues lysines 272 and 273). Mutation of these lysines abolishes homodimerization and cell adhesion, disrupts ZO-1 and E-cadherin membrane localization, reduces transepithelial resistance, and promotes epithelial-to-mesenchymal transition. GST pull-down, SPOTS analysis, site-directed mutagenesis, transepithelial resistance, immunofluorescence of junctional proteins PloS one High 18493308
2010 BVES directly interacts with VAMP3 (a SNARE protein), and disruption of BVES impairs recycling of transferrin and β1-integrin (consistent with VAMP3 dysfunction). Morpholino knockdown of BVES in Xenopus specifically inhibits transferrin receptor recycling, causing gastrulation defects; BVES-depleted cells show impaired spreading and adhesion on fibronectin. Co-immunoprecipitation, VAMP3 recycling assays (transferrin/integrin recycling), Xenopus morpholino knockdown, kymographic analysis of cell spreading The EMBO journal High 20057356
2011 BVES regulates epithelial-to-mesenchymal transition (EMT): re-expression of BVES in colorectal cancer cell lines promotes epithelial phenotype with decreased proliferation, migration, and invasion; a dominant-negative C-terminus-truncated BVES mutant in corneal epithelial cells induces mesenchymal features. These changes are associated with alterations in adherens junction and tight junction composition. Stable re-expression of BVES in CRC cell lines, dominant-negative mutant expression, orthotopic xenograft, migration/invasion assays, TJ/AJ protein localization The Journal of clinical investigation High 21911938
2011 BVES modulates RhoA signaling and ZONAB/DbpA transcriptional activity through tight junction regulation. C-terminus-truncated BVES disrupts membrane localization of endogenous BVES and ZO-1 interaction, increases RhoA activity (measured by FRET), increases ZONAB/DbpA transcriptional activity (luciferase reporter), and reduces membrane localization of GEF-H1. Stable transfection of truncated vs. wild-type BVES, FRET-based RhoA activity assay, luciferase reporter for ZONAB/DbpA, immunolocalization PloS one Medium 21283798
2012 In zebrafish, loss of BVES disrupts the PAR junctional complex, particularly atypical PKC (aPKC). Knockdown causes impaired epidermal barrier function and osmotic stress sensitivity; rescue with ZO-2/par-3/par-6/aPKC mRNAs partially restores viability and barrier function, placing BVES upstream of the PAR complex and aPKC in tight junction assembly. Morpholino knockdown in zebrafish, mRNA rescue experiments, immunofluorescence of aPKC localization The Journal of biological chemistry Medium 23019331
2013 BVES directly interacts with NDRG4, and this interaction is required for directional epicardial cell movement. BVES/NDRG4 interaction regulates trafficking of internalized fibronectin through the autocrine ECM deposition pathway. TIRF microscopy shows BVES/NDRG4 interaction is required for fusion of recycling endosomes with the basal cell surface. Protein-protein interaction assays, live TIRF microscopy of recycling endosome fusion, fibronectin recycling assay, directional migration analysis Molecular biology of the cell High 24048452
2013 POPDC1/BVES is a caveolae-associated protein: it co-localizes and co-immunoprecipitates with caveolin-3 in cardiomyocytes and co-sediments with caveolin-3 in equilibrium density gradients. Popdc1-null hearts show a 70% reduction in caveolae number, impaired Ca2+ transients, increased oxidative stress vulnerability, and loss of ischemic preconditioning. Co-immunoprecipitation with caveolin-3, equilibrium density gradient sedimentation, electron microscopy, Ca2+ transient measurement, Langendorff ischemia/reperfusion model in knockout mice PloS one High 24066022
2015 The disease-causing POPDC1(S201F) missense variant shows ~50% reduction in cAMP-binding affinity and causes impaired membrane trafficking of both POPDC1(S201F) and WT POPDC2 in patient skeletal muscle. Forced expression in HL-1 cardiomyocytes increases hyperpolarization and action potential upstroke velocity. The homologous zebrafish mutation recapitulates cardiac arrhythmia and skeletal muscle phenotypes. cAMP-binding affinity assay (S201F vs WT), immunohistochemistry of patient muscle for membrane trafficking, HL-1 cell electrophysiology, zebrafish knockin model The Journal of clinical investigation High 26642364
2016 BVES interacts with PR61α, a PP2A regulatory subunit, identified by yeast two-hybrid screen and validated mechanistically. This interaction mediates c-Myc protein destruction: loss of BVES leads to increased c-Myc levels and Wnt activation, promoting inflammatory tumourigenesis in vivo. Yeast two-hybrid screen, mechanistic studies in multiple cell lines, Bves-/- mouse AOM/DSS tumourigenesis model, molecular analysis of c-Myc and Wnt pathway Gut Medium 28389570
2016 BVES loss in cardiomyocytes under serum deprivation upregulates the pro-apoptotic protein Bnip3 and reduces Rac1-GTPase activity and Akt phosphorylation. Combined Popdc1/Bves and Bnip3 silencing attenuates cell injury; chromatin immunoprecipitation shows increased FoxO3 binding to the Bnip3 promoter, while NFκB is excluded from nuclei and shows decreased Bnip3 promoter binding in BVES-deficient cells. siRNA-mediated gene silencing, Rac1 GTPase activity assay, Western blot for Akt phosphorylation, chromatin immunoprecipitation (ChIP) for FoxO3 and NFκB at Bnip3 promoter Journal of cellular biochemistry Medium 27886395
2009 Overexpression of BVES in trabecular meshwork cells increases tight junction formation (increased occludin, cingulin, ZO-1) and decreases RhoA activation (FRET assay) and myosin light chain phosphorylation (MLC-p), establishing a regulatory pathway upstream of RhoA in these cells. Stable transfection/overexpression, FRET-based RhoA activity assay, Western blot for MLC-p, transepithelial resistance, TJ protein expression Investigative ophthalmology & visual science Medium 19628742
2022 POPDC1 scaffolds a complex of adenylyl cyclase 9 (AC9) and TREK-1 potassium channels in heart. TREK-1 binds the AC9:POPDC1 complex and co-purifies in a POPDC1-dependent manner with AC9 activity. The AC9:POPDC1 interaction is cAMP-independent, but TREK-1 association with the complex is reduced upon β-adrenergic receptor stimulation. AC9 activity is required for βAR-mediated reduction of TREK-1 complex formation and for reversing POPDC1 enhancement of TREK-1 currents. Adcy9 knockout mice show bradycardia and stress-induced heart rate variability. Co-immunoprecipitation, co-purification assays, electrophysiology (TREK-1 currents), Adcy9 knockout mouse model with heart rate recording, β-adrenergic receptor stimulation experiments EMBO reports High 36254885
2020 POPDC1 and POPDC2 interact with XIRP1 (Xin actin binding repeat-containing protein 1) and actin, identified by proteomic pull-down from human skeletal myotubes. The POPDC1-XIRP1 interaction was confirmed in adult rat heart extracts. Both POPDC1/2 and XIRP1 co-localize at intercalated discs and T-tubules in adult heart. Bead-based pulldown with proteomic analysis, co-immunoprecipitation from adult rat heart, immunolocalization with new monoclonal antibodies BMC molecular and cell biology Medium 33261556
2021 BVES is a novel interacting protein of ANO5: identified by proximity labeling (BioID2) mass spectrometry and confirmed by co-immunoprecipitation. The N-terminus of ANO5 mediates interaction with the C-terminus of BVES. ANO5 and BVES co-localize at the ER membrane in muscle cells. Genome editing-mediated disruption of either ANO5 or BVES significantly suppresses C2C12 myoblast differentiation. BioID2 proximity labeling, mass spectrometry, co-immunoprecipitation, co-localization, CRISPR/genome editing knockout with differentiation assay Cell & bioscience Medium 34963485
2023 BVES functions as a negative feedback regulator of adenylyl cyclase 9 (ADCY9)-mediated cAMP signaling in skeletal muscle. BVES interacts with and negatively regulates ADCY9's activity. BVES deletion increases PKA signaling, promoting FoxO-mediated ubiquitin-proteasome degradation and autophagy. Viral BVES re-expression in Bves-deficient muscle reverses these defects. BVES knockout mice, co-immunoprecipitation of BVES-ADCY9, cAMP/PKA activity assays, AAV-mediated rescue, FoxO pathway analysis, autophagy markers Nature communications High 36997581
2022 In BVES-knockout mice, BVES maintains vascular smooth muscle cell (VSMC) contractile phenotype through Dusp1-dependent suppression of p38MAPK and ERK1/2. BVES knockdown reduces Dusp1 expression and enhances p38MAPK and ERK1/2 activation; VSMC-specific Bves and Dusp1 overexpression in aortic grafts attenuates neointimal lesion formation. RNA sequencing, in vitro knockdown/overexpression in VSMCs, in vivo rat aortic graft model with VSMC-specific Bves overexpression, p38MAPK/ERK1/2 phosphorylation Western blot Atherosclerosis Medium 36037759
2024 POPDC1 dysfunction causes AV node dysfunction: popdc1 mutant and knockout zebrafish show reduced heart rate, altered AV delay, slower action potential upstroke, and abnormal calcium transient duration. In adult popdc1 mutant hearts, β-adrenergic receptor stimulation with isoproterenol worsens AV block and alters calcium handling, demonstrating SNS-dependent arrhythmogenesis. Functional fluorescent analysis (action potential and calcium transient imaging) in zebrafish larvae and adult isolated hearts, isoproterenol stimulation, popdc1 knockin and knockout zebrafish Genes Medium 38540339
2022 Mice lacking POPDC1 show PKA-dependent enhancement in CA1 hippocampal long-term potentiation (LTP) in response to weaker stimulation paradigms and enhanced forskolin-induced potentiation, identifying POPDC1 as a negative regulator of hippocampal synaptic plasticity via cAMP-PKA-PDE signaling. Popdc1 knockout mice, acute hippocampal slice electrophysiology (LTP induction protocols), pharmacological PKA manipulation Cerebral cortex (New York, N.Y. : 1991) Medium 34937090

Source papers

Stage 0 corpus · 61 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 bves: A novel gene expressed during coronary blood vessel development. Developmental biology 86 10208750
2001 Bves: prototype of a new class of cell adhesion molecules expressed during coronary artery development. Development (Cambridge, England) 85 11493530
2015 POPDC1(S201F) causes muscular dystrophy and arrhythmia by affecting protein trafficking. The Journal of clinical investigation 72 26642364
2005 Bves modulates epithelial integrity through an interaction at the tight junction. Journal of cell science 72 16188940
2011 BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma. The Journal of clinical investigation 64 21911938
2008 Bves directly interacts with GEFT, and controls cell shape and movement through regulation of Rac1/Cdc42 activity. Proceedings of the National Academy of Sciences of the United States of America 57 18541910
2003 Membrane topology of Bves/Pop1A, a cell adhesion molecule that displays dynamic changes in cellular distribution during development. The Journal of biological chemistry 50 12815060
2010 Frequent silencing of popeye domain-containing genes, BVES and POPDC3, is associated with promoter hypermethylation in gastric cancer. Carcinogenesis 48 20627872
2016 BVES regulates c-Myc stability via PP2A and suppresses colitis-induced tumourigenesis. Gut 44 28389570
2010 Identification of a novel Bves function: regulation of vesicular transport. The EMBO journal 43 20057356
2015 Netrin-1 promotes cell migration and invasion by down-regulation of BVES expression in human hepatocellular carcinoma. American journal of cancer research 42 26101705
2013 Popeye domain containing 1 (Popdc1/Bves) is a caveolae-associated protein involved in ischemia tolerance. PloS one 41 24066022
2013 Bves and NDRG4 regulate directional epicardial cell migration through autocrine extracellular matrix deposition. Molecular biology of the cell 40 24048452
2004 Developmental expression of Pop1/Bves. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 39 14966204
2011 Bves modulates tight junction associated signaling. PloS one 35 21283798
2004 Bves is expressed in the epithelial components of the retina, lens, and cornea. Investigative ophthalmology & visual science 31 15277466
2009 Inhibition of RhoA signaling with increased Bves in trabecular meshwork cells. Investigative ophthalmology & visual science 30 19628742
2023 Peptide encoded by lncRNA BVES-AS1 promotes cell viability, migration, and invasion in colorectal cancer cells via the SRC/mTOR signaling pathway. PloS one 29 37347740
2009 Bves: ten years after. Histology and histopathology 29 19337975
2008 Identification of a novel intracellular interaction domain essential for Bves function. PloS one 29 18493308
2014 BVES inhibition triggers epithelial-mesenchymal transition in human hepatocellular carcinoma. Digestive diseases and sciences 28 24442236
1999 Cloning and expression of hbves, a novel and highly conserved mRNA expressed in the developing and adult heart and skeletal muscle in the human. Mammalian genome : official journal of the International Mammalian Genome Society 28 10441744
2006 Characterization of Bves expression during mouse development using newly generated immunoreagents. Developmental dynamics : an official publication of the American Association of Anatomists 27 16538658
2019 Muscular dystrophy with arrhythmia caused by loss-of-function mutations in BVES. Neurology. Genetics 26 31119192
2007 Blood vessel/epicardial substance (bves) expression, essential for embryonic development, is down regulated by Grk/EFGR signalling. The International journal of developmental biology 26 17183463
2006 Bves, a member of the Popeye domain-containing gene family. Developmental dynamics : an official publication of the American Association of Anatomists 26 16444674
2016 BVES Regulates Intestinal Stem Cell Programs and Intestinal Crypt Viability after Radiation. Stem cells (Dayton, Ohio) 24 26891025
2004 Bves expression during avian embryogenesis. Developmental dynamics : an official publication of the American Association of Anatomists 22 14991721
2012 Blood vessel epicardial substance (Bves) regulates epidermal tight junction integrity through atypical protein kinase C. The Journal of biological chemistry 20 23019331
2018 BVES is required for maintenance of colonic epithelial integrity in experimental colitis by modifying intestinal permeability. Mucosal immunology 19 29907869
2001 Production of monoclonal antibodies against chicken Pop1 (BVES). Hybridoma and hybridomics 19 11839256
2022 Proteomic and morphological insights and clinical presentation of two young patients with novel mutations of BVES (POPDC1). Molecular genetics and metabolism 18 35660068
2019 Ten years of research on the role of BVES/ POPDC1 in human disease: a review. OncoTargets and therapy 16 30863095
2017 POPDC1 is suppressed in human breast cancer tissues and is negatively regulated by EGFR in breast cancer cell lines. Cancer letters 16 28807821
2017 Dysregulation of POPDC1 promotes breast cancer cell migration and proliferation. Bioscience reports 15 28954821
2022 POPDC1 scaffolds a complex of adenylyl cyclase 9 and the potassium channel TREK-1 in heart. EMBO reports 14 36254885
2020 Two Japanese LGMDR25 patients with a biallelic recurrent nonsense variant of BVES. Neuromuscular disorders : NMD 14 32684383
2016 Popdc1/Bves Functions in the Preservation of Cardiomyocyte Viability While Affecting Rac1 Activity and Bnip3 Expression. Journal of cellular biochemistry 13 27886395
2013 Mutational and functional analysis of the BVES gene coding region in Chinese patients with non-syndromic tetralogy of Fallot. International journal of molecular medicine 13 23403794
2022 A novel biallelic variant in the Popeye domain-containing protein 1 (POPDC1) underlies limb girdle muscle dystrophy type 25. Clinical genetics 11 36155908
2018 Blood Vessel Epicardial Substance (BVES) in junctional signaling and cancer. Tissue barriers 11 30307367
2021 The Transition from Gastric Intestinal Metaplasia to Gastric Cancer Involves POPDC1 and POPDC3 Downregulation. International journal of molecular sciences 10 34069715
2020 An interaction of heart disease-associated proteins POPDC1/2 with XIRP1 in transverse tubules and intercalated discs. BMC molecular and cell biology 10 33261556
2022 Cell adhesion molecule BVES functions as a suppressor of tumor cells extrusion in hepatocellular carcinoma metastasis. Cell communication and signaling : CCS 9 36123685
2021 BVES is a novel interactor of ANO5 and regulates myoblast differentiation. Cell & bioscience 9 34963485
2022 Mice Lacking the cAMP Effector Protein POPDC1 Show Enhanced Hippocampal Synaptic Plasticity. Cerebral cortex (New York, N.Y. : 1991) 8 34937090
2022 Bves maintains vascular smooth muscle cell contractile phenotype and protects against transplant vasculopathy via Dusp1-dependent p38MAPK and ERK1/2 signaling. Atherosclerosis 8 36037759
2022 Systemic AAV9.BVES delivery ameliorates muscular dystrophy in a mouse model of LGMDR25. Molecular therapy : the journal of the American Society of Gene Therapy 6 36433649
2021 The role of Popeye domain-containing protein 1 (POPDC1) in the progression of the malignant phenotype. British journal of pharmacology 6 33533478
2021 BVES-AS1 inhibits the malignant behaviors of colon adenocarcinoma cells via regulating BVES. Cell biology international 6 34003551
2024 BVES-AS1 suppresses the colorectal cancer progression via the miR-1269a/b-SVEP1-PI3K/AKT axis. Advances in clinical and experimental medicine : official organ Wroclaw Medical University 5 38239081
2023 Defective BVES-mediated feedback control of cAMP in muscular dystrophy. Nature communications 5 36997581
2020 BVES downregulation in non-syndromic tetralogy of fallot is associated with ventricular outflow tract stenosis. Scientific reports 5 32843646
2023 MBNL1‑AS1 attenuates tumor cell proliferation by regulating the miR‑29c‑3p/BVES signal in colorectal cancer. Oncology reports 4 37711058
2019 The Functional Polymorphism R129W in the BVES Gene Is Associated with Sporadic Tetralogy of Fallot in the Han Chinese Population. Genetic testing and molecular biomarkers 4 31386585
2022 Modulation of POPDC1 Expression by Phenothiazine and Trifluoperazine Suppress Colon Cancer Growth and Migration. Asian Pacific journal of cancer prevention : APJCP 3 36037145
2024 miR-665-Mediated Regulation of AHCYL2 and BVES Genes in Recurrent Implantation Failure. Genes 2 38397233
2024 POPDC1 Variants Cause Atrioventricular Node Dysfunction and Arrhythmogenic Changes in Cardiac Electrophysiology and Intracellular Calcium Handling in Zebrafish. Genes 2 38540339
2025 The BVES Gene Regulates the Homeostasis of Deer Antler Mesenchymal Stem Cells Through Wnt Signaling. Biology 0 41007355
2024 Dysregulated expression of IGSF11-AS1 and BVES-AS in azoospermia and its correlation with serum hormone levels. Biomarkers in medicine 0 38881522
2024 LncRNA GAS5 regulates the inflammatory response in inflammatory bowel disease via targeting the miR-23a-3p/BVES axis. Central-European journal of immunology 0 39944256

Missed literature

Know a paper Affinage missed for POPDC1? Flag it for the maintainers and the community.

No submissions yet.