Affinage

OCLN

Occludin · UniProt Q16625

Round 2 corrected
Length
522 aa
Mass
59.1 kDa
Annotated
2026-04-29
50 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Occludin is a four-transmembrane MARVEL-domain tight junction protein that regulates paracellular permeability, particularly the large-channel pathway controlling macromolecule flux, through its dynamic residency at tight junctions and phosphorylation-dependent trafficking (PMID:21415414, PMID:18474622). Its long COOH-terminal cytoplasmic tail directly binds ZO-1, ZO-2, ZO-3, and F-actin, anchoring it to the cortical cytoskeleton, while phosphorylation at Ser-490 drives ubiquitination and endosomal trafficking that increases vascular permeability in response to VEGF (PMID:7798316, PMID:9792688, PMID:19478092). Occludin serves as an essential hepatitis C virus co-entry factor through its second extracellular loop and MARVEL domain, is transcriptionally repressed by Snail during epithelial-mesenchymal transition, and is post-transcriptionally downregulated by miR-122 and miR-144 (PMID:19182773, PMID:12668723, PMID:25302477, PMID:29258088). Occludin also undergoes autophagosomal degradation triggered by pneumococcal StkP-mediated BECN1 phosphorylation, contributing to alveolar barrier disruption during infection (PMID:38497494).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1994 High

    The molecular basis of occludin's tight junction localization was established by demonstrating that its COOH-terminal cytoplasmic domain directly binds ZO-1, resolving how a transmembrane protein is tethered at the junctional plaque.

    Evidence Deletion mutant transfection in epithelial cells and GST-pulldown with recombinant ZO-1

    PMID:7798316

    Open questions at the time
    • Binding affinity and stoichiometry of the occludin–ZO-1 interaction were not determined
    • Whether ZO-1 binding is required for occludin function versus merely localization was unclear
  2. 1998 High

    ZO-1 was shown to function as a molecular bridge connecting occludin to cortical actin, with additional scaffolding provided by ZO-3, establishing the tripartite architecture of the tight junction plaque.

    Evidence In vitro binding/cosedimentation assays and fragment transfection in MDCK cells for ZO-1; affinity assays and immunoelectron microscopy for ZO-3

    PMID:9531559 PMID:9792688

    Open questions at the time
    • Structural basis of the ZO-1 bridging function was not resolved
    • Relative contributions of ZO-2 versus ZO-3 to occludin anchoring remained unclear
  3. 1999 High

    Occludin was found to bind F-actin directly in addition to its indirect linkage through ZO proteins, and ZO-1·ZO-2 and ZO-1·ZO-3 were shown to exist as separate dimeric complexes rather than a single trimeric scaffold, refining the junctional plaque model.

    Evidence Actin cosedimentation with recombinant protein and co-IP from MDCK cells

    PMID:10575001

    Open questions at the time
    • Functional consequence of direct occludin–actin binding was not tested
    • Whether direct actin binding is regulated by phosphorylation was unknown
  4. 2002 High

    Tyrosine phosphorylation was identified as a regulatory switch for occludin–ZO-1 association and tight junction integrity, linking oxidative stress signaling to barrier disruption.

    Evidence Oxidative stress in Caco-2 monolayers with co-IP, fractionation, TER measurement, and genistein rescue

    PMID:12169098

    Open questions at the time
    • Specific tyrosine residues phosphorylated were not identified
    • The kinase(s) responsible were not determined
  5. 2003 High

    Snail was shown to directly repress occludin transcription by binding E-box elements in its promoter, providing the first transcriptional mechanism coupling EMT to tight junction dissolution.

    Evidence Snail overexpression, promoter reporters, and EMSA in mouse epithelial cells

    PMID:12668723

    Open questions at the time
    • Whether other EMT transcription factors also target OCLN was not addressed
    • Chromatin-level regulation was not examined
  6. 2008 High

    FRAP experiments revealed that occludin is a highly dynamic component of the tight junction (71% mobile fraction) in contrast to the largely immobile claudin-1, establishing that the tight junction undergoes constitutive remodeling driven by occludin turnover.

    Evidence Quantitative FRAP with mathematical modeling in live confluent MDCK monolayers

    PMID:18474622

    Open questions at the time
    • Molecular determinants controlling occludin's high mobility were not identified
    • Whether dynamic exchange is required for barrier function was not tested
  7. 2009 High

    Occludin was identified as an essential HCV co-entry factor, with species-specific determinants mapped to the second extracellular loop, answering why murine cells resist HCV infection and establishing OCLN alongside CD81, SR-BI, and CLDN1 as the minimal receptor complex.

    Evidence cDNA library complementation in murine cells, HCVpp/HCVcc assays, siRNA knockdown, domain-swap chimeras

    PMID:19052094 PMID:19182773

    Open questions at the time
    • Whether occludin directly contacts viral particles or acts indirectly was unresolved
    • The step in the entry cascade requiring occludin was not pinpointed
  8. 2009 High

    VEGF-induced Ser-490 phosphorylation was shown to trigger occludin ubiquitination and endosomal trafficking via Epsin-1, Eps15, and Hrs, providing a complete signaling-to-trafficking mechanism for vascular permeability regulation.

    Evidence Site-directed mutagenesis (S490A), occludin–ubiquitin chimera, co-IP, permeability assays in endothelial cells

    PMID:19478092

    Open questions at the time
    • The E3 ubiquitin ligase responsible for occludin ubiquitination was not identified
    • Whether this pathway operates in non-endothelial epithelia was untested
  9. 2010 High

    Systematic isoform characterization demonstrated that MARVEL domain integrity and membrane localization are required for occludin's HCV co-receptor function, and identification of MarvelD3 defined the TAMP family with partially redundant barrier roles.

    Evidence RT-PCR isoform cloning from human liver with infectivity assays; siRNA/FRAP/EM for TAMP family analysis

    PMID:20164257 PMID:20463075

    Open questions at the time
    • Structural basis of MARVEL domain function in HCV entry was unknown
    • Extent of TAMP redundancy in vivo was not determined
  10. 2011 High

    Selective knockdown in vitro and in vivo demonstrated that occludin specifically controls the large-channel paracellular pathway for macromolecule flux without affecting ion permeability (TER), resolving its distinct functional role from claudins.

    Evidence siRNA in Caco-2 monolayers and in vivo mouse intestinal perfusion with size-graded probes

    PMID:21415414

    Open questions at the time
    • Structural mechanism by which occludin controls large-channel permeability was not defined
    • Whether this pathway is regulated dynamically by phosphorylation was not tested
  11. 2014 High

    Post-transcriptional regulation of OCLN was established by identifying miR-122 and later miR-144 as direct repressors targeting the OCLN 3'UTR, linking microRNA networks to barrier integrity and HCV susceptibility.

    Evidence Dual-luciferase 3'UTR reporter assays, miRNA mimic/inhibitor, protein quantification, functional entry and permeability assays

    PMID:25302477 PMID:29258088

    Open questions at the time
    • Relative contribution of miR-122-mediated OCLN repression versus its direct proviral role in HCV replication was not disentangled
    • Whether these miRNAs regulate OCLN in vivo at the BBB was unknown
  12. 2024 High

    A pathogen-driven degradation mechanism was uncovered: pneumococcal StkP kinase phosphorylates BECN1 to initiate autophagosomal degradation of occludin, establishing autophagy as a distinct pathway for barrier disruption during bacterial infection.

    Evidence Proteomics, co-IP, phosphorylation site identification, autophagy inhibitors, BECN1 mutants, CRISPR KO of stkP, in vivo mouse infection

    PMID:38497494

    Open questions at the time
    • Whether occludin is a direct autophagy cargo receptor substrate or is degraded indirectly was not resolved
    • Generalizability to other bacterial infections was untested
  13. 2025 Medium

    Occludin's COOH-terminus was found to link tight junction cargo to the dynein motor via its light intermediate chain, with Ser-471 phosphorylation required for motor engagement and Ser-490 phosphorylation required for trafficking; exon 5 deletion causes embryonic lethality, demonstrating that occludin is essential for development.

    Evidence Co-IP, site-directed mutagenesis, endothelial proliferation assays, collateral angiogenesis model, exon 5-targeted gene deletion (preprint)

    PMID:bio_10.1101_2025.06.12.659326

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Structural details of occludin–dynein LIC interface are unknown
    • Whether dynein-mediated trafficking is relevant to all occludin-dependent barrier functions was not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions remain: the E3 ubiquitin ligase mediating VEGF-induced occludin ubiquitination has not been identified, the structural basis of the MARVEL domain's roles in barrier function and HCV entry is unresolved, and whether occludin's newly described roles in innate immunity and mitochondrial dynamics at the BBB operate through its canonical junctional function or represent junction-independent signaling remains to be dissected.
  • E3 ligase identity unknown
  • No high-resolution structure of full-length occludin
  • Junction-independent signaling mechanisms are poorly defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 4 GO:0098631 cell adhesion mediator activity 4 GO:0001618 virus receptor activity 3
Localization
GO:0005886 plasma membrane 6 GO:0005856 cytoskeleton 2 GO:0005768 endosome 1
Pathway
R-HSA-1500931 Cell-Cell communication 5 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2 R-HSA-5653656 Vesicle-mediated transport 1 R-HSA-9612973 Autophagy 1
Partners
CLDN1MARVELD3TGFBR1TJP1TJP2TJP3
Complex memberships
Tight junction plaque (ZO-1·occludin·ZO-3 scaffold)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 Occludin's long COOH-terminal cytoplasmic domain (domain E, specifically the ~150 aa subdomain E358/504) is necessary for its localization at tight junctions and directly associates with ZO-1 (and ZO-2 complex) in vitro, suggesting that cytoskeletal anchoring through ZO-1 is required for occludin's tight junction localization. Deletion mutant transfection in epithelial cells, GST-fusion protein pulldown, in vitro binding assay with recombinant ZO-1 The Journal of cell biology High 7798316
1996 Occludin is a conserved integral membrane tight junction protein across mammals (human, mouse, dog, rat-kangaroo); mammalian homologues share ~90% amino acid identity with each other but only ~50% with chicken, establishing the conserved four-transmembrane topology across species. cDNA cloning and sequence analysis across species The Journal of cell biology Medium 8601611
1998 ZO-1 links occludin to the actin cytoskeleton: occludin interacts with a specific domain in the N-terminal (MAGUK-like) half of ZO-1, while the C-terminal proline-rich half of ZO-1 cosediments with F-actin, placing ZO-1 as a molecular bridge between the transmembrane occludin and cortical actin. Epitope-tagged ZO-1 fragment transfection in MDCK cells, in vitro binding assays, co-sedimentation The Journal of biological chemistry High 9792688
1998 ZO-3 directly interacts with both ZO-1 and the cytoplasmic domain of occludin (but not ZO-2) in vitro affinity assays, and colocalizes with ZO-1 at tight junctions, identifying ZO-3 as an additional occludin-binding scaffold at the tight junction. In vitro affinity binding assays with recombinant proteins, immunofluorescence, immunoelectron microscopy The Journal of cell biology High 9531559
1999 Occludin directly interacts with F-actin in vitro, and ZO-2 also binds directly to occludin; in situ ZO-1, ZO-2, and ZO-3 exist primarily as independent ZO-1·ZO-2 and ZO-1·ZO-3 complexes rather than a trimeric complex, defining the molecular architecture of the tight junction plaque. Actin cosedimentation assays with purified recombinant proteins, co-immunoprecipitation from MDCK cells, immunofluorescence in cytochalasin D-treated cells The Journal of biological chemistry High 10575001
2002 Oxidative stress induces tyrosine phosphorylation of occludin, causing dissociation of occludin–ZO-1 complexes from the cytoskeletal fraction and redistribution from intercellular junctions; tyrosine kinase inhibitor genistein prevents these effects and preserves transepithelial resistance, establishing that tyrosine phosphorylation of occludin regulates its association with ZO-1 and tight junction integrity. Caco-2 monolayer oxidative stress model, co-immunoprecipitation, Triton-insoluble fractionation, transepithelial resistance measurement, pharmacological inhibition The Biochemical journal High 12169098
2003 Snail transcription repressor directly binds to E-boxes in the promoters of occludin (and claudin) genes, repressing their transcription during epithelial-mesenchyme transition (EMT), thereby directly coupling EMT to loss of tight junction proteins at the transcriptional level. Snail overexpression in mouse epithelial cells, promoter reporter assays, electrophoretic mobility shift assay (EMSA), qRT-PCR and western blot for mRNA and protein Journal of cell science High 12668723
2005 Occludin physically interacts with TGF-β type I receptor (identified by LUMIER technology) and regulates its localization, thereby facilitating efficient TGF-β-dependent dissolution of tight junctions during epithelial-to-mesenchymal transition. LUMIER (luminescence-based mammalian interactome mapping) high-throughput protein-protein interaction assay, functional TGF-β signaling studies Science Medium 15761153
2008 By FRAP analysis in live confluent MDCK monolayers, the majority of occludin (71%) diffuses rapidly within the tight junction membrane with a diffusion constant of ~0.011 µm²/s, in contrast to claudin-1 which is largely stable (76% immobile), demonstrating that the tight junction undergoes constant remodeling with occludin as a highly dynamic component. Fluorescence recovery after photobleaching (FRAP) in live confluent MDCK monolayers, mathematical modeling of diffusion The Journal of cell biology High 18474622
2009 Human occludin is an essential HCV cell entry factor: overexpression of human OCLN in otherwise non-permissive murine cells renders them infectable with HCV pseudoparticles (HCVpp), and siRNA knockdown of OCLN in permissive human cells impairs both HCVpp and HCVcc infection. Together with CD81, SR-BI, and CLDN1, OCLN is required for HCV entry; species-specific determinants of OCLN were mapped to its second extracellular loop. cDNA library screening, HCVpp and HCVcc infection assays in murine cells expressing human OCLN, siRNA knockdown in permissive human cells, chimeric/domain-swap constructs Nature High 19182773
2009 VEGF-A specifically down-regulates both claudin-5 and occludin protein and mRNA in brain microvascular endothelial cells; recombinant occludin expressed from the same promoter as CLN-5 was not protective against VEGF-induced paracellular permeability increase, whereas CLN-5 was, indicating that occludin loss contributes to but is not the primary determinant of VEGF-mediated BBB breakdown. Brain microvascular endothelial cell cultures, in vivo microinjection in mouse cerebral cortex, recombinant protein overexpression, permeability assays Proceedings of the National Academy of Sciences of the United States of America High 19174516
2009 VEGF treatment of endothelial cells induces phosphorylation of occludin on Ser-490 and subsequent ubiquitination; phosphorylated/ubiquitinated occludin traffics from cell borders to early and late endosomes, and occludin interacts with ubiquitin-interacting motif (UIM) proteins Epsin-1, Eps15, and Hrs. Mutating Ser-490 to Ala suppresses VEGF-induced ubiquitination, blocks TJ protein trafficking, and prevents permeability increase; an occludin-ubiquitin chimera disrupts TJs and increases permeability without VEGF. Co-immunoprecipitation, immunocytochemistry, site-directed mutagenesis (S490A), occludin-ubiquitin chimera overexpression, permeability assays in endothelial cells The Journal of biological chemistry High 19478092
2008 Occludin (along with claudin-1) is required for HCV entry into liver cells and is downregulated during HCV infection to prevent superinfection; mutational analysis of claudin-1 showed that its tight junctional distribution is important for viral entry, supporting a model in which HCV enters from the tight junction. HCV pseudoparticle entry assays, siRNA knockdown, CLDN1 mutational analysis, HCV infection of Huh-7 cells Journal of virology High 19052094
2010 The OCLN gene produces multiple alternative splice variants in human liver; only the wild-type (WT-OCLN) and OCLN-ex7ext isoforms, which retain the MARVEL domain, are expressed on the cell membrane and are permissive for HCV infection in vitro. All other isoforms lacking the MARVEL domain are expressed cytoplasmically and are non-permissive, demonstrating that the MARVEL domain and membrane localization are required for occludin's HCV co-receptor function. RT-PCR cloning of splice variants from human liver, recombinant isoform expression, subcellular localization analysis, HCV infectivity assays in vitro Journal of virology High 20463075
2010 MarvelD3 is a novel tight junction MARVEL-domain protein related to occludin and tricellulin; FRAP and protein interaction studies show these three MARVEL proteins have distinct but overlapping functions—marvelD3 can partially compensate for occludin or tricellulin loss but cannot fully restore function, defining the tight junction-associated MARVEL protein (TAMP) family with redundant and unique contributions to epithelial barrier function. siRNA knockdown, FRAP, immunofluorescence/electron microscopy, protein interaction assays, in vivo immune activation, phylogenetic analysis Molecular biology of the cell High 20164257
2011 Selective siRNA knockdown of occludin in Caco-2 monolayers in vitro and in mouse intestine in vivo causes a preferential increase in macromolecule flux (urea, mannitol, inulin, dextran) without affecting transepithelial resistance, demonstrating that occludin specifically regulates the large-channel tight junction pathway responsible for macromolecule permeability. siRNA knockdown in Caco-2 monolayers, in vivo mouse intestinal recycling perfusion with siRNA, transepithelial resistance measurement, flux assays with size-graded probes American journal of physiology. Gastrointestinal and liver physiology High 21415414
2014 miR-122 binds directly to the 3' UTR of OCLN mRNA and down-regulates occludin protein expression; miR-122 overexpression in Huh7.5 cells reduces OCLN protein by ~80%, decreases colocalization of OCLN with CLDN at tight junctions, and reduces HCV pseudoparticle entry by ~42%, establishing miR-122 as a post-transcriptional repressor of OCLN that indirectly inhibits HCV entry. Dual-luciferase reporter assay with 3'UTR construct, miR-122 mimic/inhibitor transfection, western blot, immunofluorescence co-localization, lentiviral miR-122 overexpression, HCV pseudoparticle and VSV pseudoparticle entry assays Liver international High 25302477
2017 miR-144 directly targets OCLN and ZO1 mRNA (validated by dual-luciferase assay with mutant controls); miR-144 overexpression in IBS-D rat colonic epithelial cells decreases OCLN and ZO1 expression and enhances intestinal hyperpermeability, while inhibition of miR-144 or rescue overexpression of OCLN/ZO1 reverses hyperpermeability, establishing miR-144 as a direct post-transcriptional repressor of OCLN. miRNA microarray, qRT-PCR, western blot, ELISA, dual-luciferase assay with 3'UTR mutants, miRNA mimic/inhibitor transfection, rescue overexpression experiments in colonic epithelial cells Cellular physiology and biochemistry High 29258088
2024 S. pneumoniae releases extracellular vesicles (pEVs) containing the virulence kinase StkP; internalized StkP phosphorylates BECN1 at Ser93 and Ser96, initiating autophagy, which leads to autophagosomal degradation of OCLN and consequent alveolar epithelial barrier dysfunction. Deletion of stkP in S. pneumoniae abolishes pEV-induced OCLN degradation and protects mice from death. Proteomics of pEV cargo, co-immunoprecipitation, phosphorylation site identification, autophagy inhibitors (BafA1, CQ), BECN1 mutants, CRISPR KO of stkP, TEER measurement, in vivo mouse infection model Autophagy High 38497494
2025 The OCLN carboxy-terminus forms a complex with the light intermediate chain (LIC) of dynein, linking tight junction cargo to the minus-end-directed motor protein. Ser471 phosphorylation is required for LIC binding, while Ser490 phosphorylation is required for trafficking. Expression of the S490A mutant prevents endothelial cell proliferation and collateral angiogenesis. OCLN gene deletion targeting exon 5 (preventing both full-length and isoform 4 expression) results in embryonic lethality. Co-immunoprecipitation, site-directed mutagenesis (S471A, S490A), endothelial cell proliferation assays, collateral angiogenesis model, exon 5-targeted gene deletion (embryonic lethality phenotype) bioRxivpreprint Medium bio_10.1101_2025.06.12.659326
2025 Occludin silencing (ocln KD) in brain endothelial cells alters gene expression signatures of innate immunity including IFN-stimulated genes and the RIG-1/MAVS antiviral signaling pathway, and causes dysfunctional mitochondrial bioenergetics and autophagy; in EcoHIV-infected ocln-deficient mice, these alterations translate to worsened ischemic stroke outcomes, identifying occludin as a regulator of innate immune responses and mitochondrial dynamics in the BBB. Occludin siRNA knockdown in brain endothelial cells, gene expression profiling, mitochondrial bioenergetics assays, EcoHIV infection in ocln-deficient mice, ischemic stroke model bioRxivpreprint Medium bio_10.1101_2024.06.07.598027
2021 miR-122-5p in LPS-induced neutrophil exosomes directly targets OCLN mRNA (validated by dual-luciferase assay), downregulates OCLN expression in brain microvascular endothelial cells, and promotes apoptosis, oxidative stress, and increased permeability; OCLN overexpression partially reverses these effects. Dual-luciferase reporter assay, western blot, exosome co-culture, flow cytometry (apoptosis), ROS assays, OCLN overexpression rescue American journal of translational research Medium 34150006
2025 miR-20a overexpression in a sepsis model inhibits DUSP3 (a target of miR-20a), which in turn suppresses ubiquitination of OCLN, thereby preserving OCLN protein levels and intestinal barrier integrity; OCLN knockdown abolishes the protective effect of miR-20a overexpression, placing OCLN downstream of the miR-20a/DUSP3 axis in barrier regulation. CLP mouse sepsis model and LPS-treated NCM460 cells, miR-20a mimic/DUSP3 OE/KD/OCLN KD, western blot, RT-qPCR, ELISA, flow cytometry, immunofluorescence, HE staining In vitro cellular & developmental biology. Animal Medium 40392484

Source papers

Stage 0 corpus · 50 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 The sequence of the human genome. Science (New York, N.Y.) 8428 11181995
2007 ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage. Science (New York, N.Y.) 2519 17525332
2019 Blood-Brain Barrier: From Physiology to Disease and Back. Physiological reviews 1645 30280653
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1998 The tight junction protein ZO-1 establishes a link between the transmembrane protein occludin and the actin cytoskeleton. The Journal of biological chemistry 1142 9792688
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
1999 Direct binding of three tight junction-associated MAGUKs, ZO-1, ZO-2, and ZO-3, with the COOH termini of claudins. The Journal of cell biology 921 10601346
2020 A reference map of the human binary protein interactome. Nature 849 32296183
1994 Direct association of occludin with ZO-1 and its possible involvement in the localization of occludin at tight junctions. The Journal of cell biology 791 7798316
2009 Human occludin is a hepatitis C virus entry factor required for infection of mouse cells. Nature 728 19182773
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2003 Regulation of tight junctions during the epithelium-mesenchyme transition: direct repression of the gene expression of claudins/occludin by Snail. Journal of cell science 557 12668723
2005 High-throughput mapping of a dynamic signaling network in mammalian cells. Science (New York, N.Y.) 553 15761153
2009 VEGF-mediated disruption of endothelial CLN-5 promotes blood-brain barrier breakdown. Proceedings of the National Academy of Sciences of the United States of America 548 19174516
1998 ZO-3, a novel member of the MAGUK protein family found at the tight junction, interacts with ZO-1 and occludin. The Journal of cell biology 469 9531559
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2015 A Dynamic Protein Interaction Landscape of the Human Centrosome-Cilium Interface. Cell 433 26638075
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1999 Protein interactions at the tight junction. Actin has multiple binding partners, and ZO-1 forms independent complexes with ZO-2 and ZO-3. The Journal of biological chemistry 384 10575001
2002 Tyrosine phosphorylation and dissociation of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the cytoskeleton by oxidative stress. The Biochemical journal 345 12169098
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2011 Occludin regulates macromolecule flux across the intestinal epithelial tight junction barrier. American journal of physiology. Gastrointestinal and liver physiology 324 21415414
2009 Occludin phosphorylation and ubiquitination regulate tight junction trafficking and vascular endothelial growth factor-induced permeability. The Journal of biological chemistry 293 19478092
2008 The tight junction protein complex undergoes rapid and continuous molecular remodeling at steady state. The Journal of cell biology 276 18474622
2008 Tight junction proteins claudin-1 and occludin control hepatitis C virus entry and are downregulated during infection to prevent superinfection. Journal of virology 268 19052094
1996 Interspecies diversity of the occludin sequence: cDNA cloning of human, mouse, dog, and rat-kangaroo homologues. The Journal of cell biology 262 8601611
2010 Tight junction-associated MARVEL proteins marveld3, tricellulin, and occludin have distinct but overlapping functions. Molecular biology of the cell 260 20164257
2017 MiR-144 Increases Intestinal Permeability in IBS-D Rats by Targeting OCLN and ZO1. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 67 29258088
2020 Lactobacillus casei LC01 Regulates Intestinal Epithelial Permeability through miR-144 Targeting of OCLN and ZO1. Journal of microbiology and biotechnology 31 32807750
2010 Splicing diversity of the human OCLN gene and its biological significance for hepatitis C virus entry. Journal of virology 30 20463075
2024 Streptococcus pneumoniae extracellular vesicles aggravate alveolar epithelial barrier disruption via autophagic degradation of OCLN (occludin). Autophagy 23 38497494
2021 Exosomes containing miR-122-5p secreted by LPS-induced neutrophils regulate the apoptosis and permeability of brain microvascular endothelial cells by targeting OCLN. American journal of translational research 22 34150006
2017 Band-like calcification with simplified gyration and polymicrogyria: report of 10 new families and identification of five novel OCLN mutations. Journal of human genetics 20 28179633
2014 MiR-122 decreases HCV entry into hepatocytes through binding to the 3' UTR of OCLN mRNA. Liver international : official journal of the International Association for the Study of the Liver 18 25302477
2017 Increased cerebral expressions of MMPs, CLDN5, OCLN, ZO1 and AQPs are associated with brain edema following fatal heat stroke. Scientific reports 16 28490769
2017 Downregulation of OCLN and GAS1 in clear cell renal cell carcinoma. Oncology reports 10 28184927
2017 Comprehensive molecular screening strategy of OCLN in band-like calcification with simplified gyration and polymicrogyria. Clinical genetics 9 28386946
2020 Tree shrew bone marrow-derived mesenchymal stem cells express CD81, OCLN, and miR-122, facilitating the entire hepatitis C virus life cycle. Journal of medical virology 8 32056224
2020 A homozygote frameshift mutation in OCLN gene result in Pseudo-TORCH syndrome type I: A case report extending the phenotype with central diabetes insipidus and renal dysfunction. European journal of medical genetics 8 32240828
2017 Effect of calprotectin subunit S100A9 on the expression and methylation of OCLN in human melanoma cell line A-375. Turkish journal of biology = Turk biyoloji dergisi 6 30814850
2021 OCLN gene variants identified in three patients with severe neurodevelopmental disorder associated with epilepsy, intellectual disability and malformation of cortical development. Epileptic disorders : international epilepsy journal with videotape 4 34704946
2022 LncRNA ALDB-898 modulates intestinal epithelial cell damage caused by Clostridium perfringens type C in piglet by regulating ssc-miR-122-5p/OCLN signaling. Molecular immunology 3 35834877
2017 Alginate-embedded HuH-7 cells increase MMP-9 and reduce OCLN expression in vitro. Cancer cell international 3 28053600
2021 MiR-224-5p Targeting OCLN Promotes the Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma Cells. Urologia internationalis 1 34515239
2021 A Fetus with Congenital Microcephaly, Microphthalmia and Cataract Was Detected with Biallelic Variants in the OCLN Gene: A Case Report. Diagnostics (Basel, Switzerland) 1 34573918
2026 Testicular Gap (CX43) and Tight Junction (OCLN, CLDN3, 5 and 11) Components in the Dog Are Affected by GnRH-Mediated Downregulation. Animals : an open access journal from MDPI 0 41594443
2025 Overexpression of miR-20a targeting DUSP3 inhibits OCLN ubiquitination levels and alleviates sepsis induced intestinal barrier dysfunction. In vitro cellular & developmental biology. Animal 0 40392484