Affinage

CLDN11

Claudin-11 · UniProt O75508

Length
207 aa
Mass
22.0 kDa
Annotated
2026-06-09
55 papers in source corpus 17 papers cited in narrative 17 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

CLDN11 (oligodendrocyte-specific protein, OSP) is a claudin-family tight-junction protein that builds the parallel-array tight-junction strands of CNS myelin and Sertoli cell junctions, where it establishes the paracellular barriers required for normal nerve conduction and spermatogenesis (PMID:10612400, PMID:10225958). It self-assembles into tight-junction strands when expressed in fibroblasts and localizes specifically to the interlamellar strands of oligodendrocyte myelin and to Sertoli cell junctions, making it one of the most abundant proteins of CNS myelin (PMID:10225958, PMID:9418959). In myelin, CLDN11 acts redundantly with PLP/DM20 to maintain compact membrane wrapping and normal axon caliber, with each protein compensating for loss of the other (PMID:15886014). Beyond its structural barrier role, CLDN11 functions in a signaling complex with the tetraspanin OAP-1 and β1 integrin, and associates with the K+ channel KV3.1, to regulate oligodendrocyte progenitor proliferation and migration (PMID:11309411, PMID:16624990). In Sertoli cells, CLDN11-dependent junctions polarize the basal distribution of stem cell factor to support differentiating spermatogonia and form an immunological barrier that prevents autoimmune attack on germ cells [PMID:bio_10.1101_2024.07.16.602181]. In epithelial and cancer contexts, CLDN11 restrains cell migration and invasion by interacting through its intracellular loop and C-terminus with tubulins TUBA1B and TUBB3 to block tubulin polymerization, and its expression is controlled by promoter methylation, mRNA-stabilizing factors, and non-coding RNAs (PMID:29747653, PMID:39856555, PMID:33677577). De novo stop-loss variants in CLDN11 cause hypomyelinating leukodystrophy, consistent with its essential role in CNS myelin (PMID:33313762).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1999 High

    Establishing whether a single claudin underlies the specialized tight-junction strands of myelin and Sertoli cells answered what molecule mediates these barriers and why their loss impairs conduction and fertility.

    Evidence Osp-null knockout mice analyzed by freeze-fracture EM, electrophysiology, and behavioral phenotyping; parallel reconstitution of TJ strands in transfected fibroblasts with immunoelectron microscopy localization

    PMID:10225958 PMID:10612400

    Open questions at the time
    • Atomic/structural basis of strand formation not resolved
    • Partner claudins or accessory proteins in strands not defined here
  2. 2000 Medium

    Mapping CLDN11 expression across development clarified which lineages depend on it, refining the tissue scope of its barrier function.

    Evidence In situ hybridization, immunohistochemistry, EM-immunohistochemistry, and Western blot across prenatal and postnatal tissues

    PMID:10797530

    Open questions at the time
    • Functional roles of prenatal meningeal/cartilage/mesoderm expression not tested
    • Identity and significance of the two developmental transcripts not resolved
  3. 2001 High

    Identifying CLDN11 binding partners showed that it is not merely structural but participates in a signaling complex governing oligodendrocyte progenitor behavior.

    Evidence Yeast two-hybrid screen identifying OAP-1, reciprocal co-IP, confocal immunocytochemistry, overexpression and antibody-inhibition migration assays, and OSP-deficient oligodendrocyte migration assays

    PMID:11309411

    Open questions at the time
    • Downstream signaling output of the OSP–OAP-1–β1 integrin complex not defined
    • Stoichiometry of the ternary complex unknown
  4. 2005 High

    Double-knockout epistasis with PLP/DM20 resolved why single CLDN11 loss gives only mild myelin phenotypes, revealing functional redundancy in maintaining compact myelin.

    Evidence Cldn11/Plp double-knockout mice with EM of myelin, Western blot for compensatory expression, and neurological assessment

    PMID:15886014

    Open questions at the time
    • Molecular basis of cross-compensation unknown
    • Whether CLDN11 and PLP physically interact not established
  5. 2006 High

    Linking CLDN11 to the KV3.1 K+ channel connected junctional protein function to ionic regulation of oligodendrocyte progenitor proliferation and migration.

    Evidence Yeast two-hybrid, reciprocal co-IP, co-immunohistochemistry, Kv3.1 knockout mouse, patch-clamp, and proliferation/migration assays

    PMID:16624990

    Open questions at the time
    • Mechanism coupling channel activity to migration not defined
    • Whether KV3.1 binding modulates CLDN11 barrier function unknown
  6. 2012 Medium

    Defining the cis-regulatory region driving Sertoli-cell expression showed which DNA elements are sufficient to restore the fertility function of CLDN11.

    Evidence Transgenic rescue of Cldn11-null azoospermia with promoter-deletion mapping

    PMID:22378758

    Open questions at the time
    • Specific transcription factors binding the Sertoli enhancer not identified
    • Regulation of oligodendrocyte expression not addressed here
  7. 2018 Medium

    Discovery of CLDN11–tubulin interaction and epigenetic silencing in cancer revealed a non-junctional, cytoskeleton-directed mechanism by which CLDN11 suppresses cell migration.

    Evidence MBD-ChIP-seq, bisulfite sequencing, promoter reporter/EMSA for GATA1, co-IP plus LC-MS/MS identifying TUBA1B/TUBB3, domain mapping, and migration/invasion assays with nocodazole

    PMID:29747653

    Open questions at the time
    • Whether tubulin binding occurs in normal myelin/Sertoli contexts not tested
    • Structural basis of tubulin-polymerization blockade not resolved
  8. 2021 Medium

    Identification of de novo stop-loss variants tied CLDN11 directly to a human Mendelian myelin disease, establishing its non-redundant requirement in human CNS myelination.

    Evidence Exome sequencing of leukodystrophy patients, RNA expression analysis in patient fibroblasts, and structural prediction of the extended protein

    PMID:33313762

    Open questions at the time
    • Functional consequence of the C-terminal extension on junction assembly not experimentally shown
    • Effect on intracellular partner interactions predicted but not demonstrated
  9. 2021 Medium

    Defining a MALAT1–miR-146b-5p–CLDN11 axis explained how CLDN11 levels are post-transcriptionally tuned to maintain the intestinal mucosal barrier.

    Evidence MALAT1 knockout colitis model, dual-luciferase reporter, Ago2-RIP, miRNA mimic/inhibitor, and monolayer permeability assays

    PMID:33677577

    Open questions at the time
    • Direct CLDN11 junctional role in gut versus indirect effects not fully separated
    • Single-lab finding
  10. 2025 Medium

    Identifying IGF2BP3 as a CLDN11 mRNA stabilizer downstream of TNF-α linked inflammatory signaling to control of intestinal paracellular permeability through CLDN11.

    Evidence RNA immunoprecipitation and RNA pull-down, IGF2BP3/CLDN11 knockdown/overexpression, Caco-2 permeability assays, and AAV-mediated overexpression in an in vivo model

    PMID:39856555

    Open questions at the time
    • Whether IGF2BP3 regulates CLDN11 in CNS or testis unknown
    • Single-lab finding
  11. 2024 Medium

    Sertoli-cell knockout work resolved whether spermatogenesis failure is barrier-driven or autoimmune, showing CLDN11 polarizes SCF distribution and forms an immunological barrier.

    Evidence Cldn11 knockout crossed to immunodeficient background (genetic epistasis), serum autoantibody detection, SCF immunolocalization, and spermatogonial proliferation assays (preprint)

    PMID:bio_10.1101_2024.07.16.602181

    Open questions at the time
    • Mechanism by which CLDN11 junctions polarize SCF not defined
    • Preprint, not yet peer-reviewed
  12. 2024 Low

    Cancer studies placed CLDN11 in growth-signaling contexts (hedgehog/FOXM1 in breast cancer; fibroblast-secreted CLDN11 in gastric cancer), implicating altered CLDN11 in tumor proliferation and metastasis.

    Evidence siRNA silencing with hedgehog inhibitor in breast cancer cells and in vivo; single-cell RNA-seq and metastasis models implicating CXCR7/AKT-driven fibroblast CLDN11 in gastric cancer

    PMID:38335659 PMID:39438406

    Open questions at the time
    • No direct biochemical interaction between CLDN11 and hedgehog or secretion machinery shown
    • Context-dependent and possibly opposing roles not reconciled

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CLDN11's structural barrier activity, cytoskeletal tubulin engagement, and the various signaling outputs (PI3K/AKT, hedgehog, Notch) mechanistically integrate within a single protein remains unresolved.
  • No structural model of CLDN11 strands or partner complexes
  • Whether signaling roles are direct or secondary to barrier disruption unknown
  • Tissue-specific partner usage not systematically mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0008092 cytoskeletal protein binding 1 GO:0098631 cell adhesion mediator activity 1
Localization
GO:0005886 plasma membrane 3
Pathway
R-HSA-1266738 Developmental Biology 2 R-HSA-1500931 Cell-Cell communication 2
Partners
ITGB1KCNC1OAP-1PLP1TUBA1BTUBB3
Complex memberships
CNS myelin tight-junction (interlamellar) strandsOSP/CLDN11–OAP-1–β1 integrin complexSertoli cell tight junction

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 OSP/claudin-11 null mice lack tight junction intramembranous strands in CNS myelin and between Sertoli cells, demonstrating that CLDN11 is the mediator of parallel-array tight junction strands in these tissues, and is required for paracellular barrier formation essential for spermatogenesis and normal CNS nerve conduction. Knockout mouse (Osp-null), freeze fracture electron microscopy, electrophysiology, behavioral phenotyping Cell High 10612400
1999 OSP/claudin-11 forms tight junction strands in transfected fibroblasts, and immunoelectron microscopy localizes it specifically to interlamellar strands of oligodendrocyte myelin sheaths and to Sertoli cell TJ strands in testis, establishing that interlamellar strands are a variant of TJ strands sharing claudin-11 with Sertoli cell junctions. Transfection of fibroblasts (TJ strand formation assay), immunofluorescence microscopy, immunoelectron microscopy, Northern blot The Journal of cell biology High 10225958
2001 OSP/claudin-11 forms a ternary complex with OAP-1 (a novel tetraspanin) and β1 integrin; this complex regulates oligodendrocyte proliferation and migration. OAP-1 was identified by yeast two-hybrid screen, confirmed by co-immunoprecipitation and confocal immunocytochemistry. Overexpression of OSP/claudin-11 or OAP-1 induced proliferation, and antibodies against each component or loss of OSP/claudin-11 impaired primary oligodendrocyte migration. Yeast two-hybrid screen, co-immunoprecipitation, confocal immunocytochemistry, overexpression assays, antibody inhibition of migration, OSP-deficient primary oligodendrocyte migration assay The Journal of cell biology High 11309411
2005 In OSP/claudin-11 and PLP/DM20 double-knockout mice, CNS myelin compaction is severely disrupted and axon diameters are markedly reduced, while single knockouts have mild phenotypes. Furthermore, loss of one protein leads to compensatory upregulation of the other, demonstrating functional redundancy and an essential structural role for both proteins in maintaining compact myelin. Double-knockout mouse generation, electron microscopy of myelin, Western blot (compensatory expression), neurological assessment Molecular and cellular neurosciences High 15886014
2006 K+ channel KV3.1 associates with OSP/claudin-11; this interaction was identified by yeast two-hybrid and confirmed by co-immunoprecipitation and co-immunohistochemistry. KV3.1-specific currents and OSP/claudin-11 cooperate to regulate oligodendrocyte progenitor cell proliferation and migration, and KV3.1 knockout mice show decreased axon diameter and thinner myelin. Yeast two-hybrid, co-immunoprecipitation, co-immunohistochemistry, Kv3.1 knockout mouse, patch-clamp electrophysiology, proliferation and migration assays American journal of physiology. Cell physiology High 16624990
2000 During prenatal development CLDN11 is expressed in meninges, cartilage-adjacent areas, and mesoderm; postnatally, expression is restricted to oligodendrocytes (from early progenitor through mature stages) and testis. Electron microscopic immunohistochemistry localizes OSP/claudin-11 to laminar myelin in adult CNS. Two developmentally regulated transcripts were detected by Western blot. In situ hybridization, immunohistochemistry, electron microscopic immunohistochemistry, Western blot Journal of neuroscience research Medium 10797530
1997 OSP is the third most abundant protein in CNS myelin, comprising approximately 7% of total myelin protein, and is enriched >30-fold in purified myelin. It is not a glycoprotein based on negative reactivity with agglutinins and HNK1 antibody. Immunohistochemistry, biochemical fractionation/purification of myelin, Western blot with peptide antibody Journal of neuroscience research Medium 9418959
2012 A 5 kb promoter/enhancer region upstream of exon 1 of Cldn11 is sufficient to rescue azoospermia in Cldn11-null mice via transgenic complementation, and cis-regulatory elements sufficient for Sertoli cell-specific expression are located within 2 kb upstream of the Cldn11 transcription start site. Transgenic mouse rescue of Cldn11-null azoospermia, promoter-deletion transgenic analysis Biology of reproduction Medium 22378758
2018 CLDN11 is epigenetically silenced by promoter hypermethylation in nasopharyngeal carcinoma (NPC); DNA methylation inhibits binding of the transcription activator GATA1 to the CLDN11 promoter region −62 to −53. Re-expression of CLDN11 reduces cell migration and invasion. Co-immunoprecipitation and LC-MS/MS identified tubulin alpha-1b (TUBA1B) and beta-3 (TUBB3) as CLDN11-interacting proteins; CLDN11 interacts through its intracellular loop and C-terminus and blocks tubulin polymerization to inhibit cell migration. MBD-ChIP sequencing, bisulfite sequencing, promoter reporter assay, EMSA, CLDN11 overexpression + migration/invasion assays, Co-immunoprecipitation, LC-MS/MS proteomics, nocodazole treatment Journal of experimental & clinical cancer research Medium 29747653
2021 De novo stop-loss variants in CLDN11 (c.622T>C and c.622T>G) cause hypomyelinating leukodystrophy. The c.622T>C variant does not trigger nonsense-mediated decay in fibroblasts, indicating translation of an extended protein predicted to form an α-helix not incorporated into the cytoplasmic membrane, potentially perturbing CLDN11 interactions with intracellular proteins. Exome sequencing, RNA expression analysis in patient fibroblasts, protein structure prediction Brain : a journal of neurology Medium 33313762
2021 MALAT1 sequesters miR-146b-5p to maintain CLDN11 expression in intestinal epithelial cells; MALAT1 knockout mice are hypersensitive to DSS-induced colitis and show loss of CLDN11 at apical junction complexes. The MALAT1–miR-146b-5p–CLDN11 axis regulates intestinal mucosal barrier integrity. MALAT1 knockout mouse colitis model, lentiviral transfection, miRNA mimic/inhibitor, dual-luciferase reporter assay, Ago2-RIP, monolayer permeability assay, Western blot Journal of Crohn's & colitis Medium 33677577
2025 CLDN11 mRNA stability in intestinal epithelial cells is regulated by IGF2BP3, which binds CLDN11 mRNA directly (validated by RNA immunoprecipitation and RNA pull-down). TNF-α treatment downregulates IGF2BP3 and consequently destabilizes CLDN11 mRNA, increasing intestinal paracellular permeability; CLDN11 overexpression reduces Caco-2 monolayer permeability and knockdown increases it. RNA immunoprecipitation (RIP), RNA pull-down assay, IGF2BP3/CLDN11 knockdown and overexpression, Caco-2 permeability assay, adeno-associated virus-mediated CLDN11 overexpression in obesity-related SAP model Molecular medicine Medium 39856555
2024 CLDN11 deficiency in breast cancer cells activates the hedgehog signaling pathway, leading to upregulation of FOXM1 and sustained tumor proliferation and migration; in vivo, hedgehog signaling blockade suppressed tumor progression caused by CLDN11 silencing. CLDN11 siRNA silencing in MCF-7 and MDA-MB-231 cells, hedgehog pathway inhibitor in vivo, proliferation and migration assays, Western blot Journal of molecular histology Low 39438406
2025 CLDN11 promotes granulosa cell proliferation via the PI3K/AKT signaling pathway, increasing expression of CCND1 and PCNA; CLDN11 knockdown inhibited viability and increased apoptosis of granulosa cells, while AAV-mediated CLDN11 overexpression reversed the PCOS-like phenotype in a rat model. CLDN11 siRNA knockdown and overexpression in rat granulosa cells, PI3K/AKT pathway analysis, AAV-mediated overexpression in rat PCOS model, Western blot, cell viability and apoptosis assays Scientific reports Low 39875531
2024 CXCR7 activation of the AKT pathway in fibroblasts promotes CLDN11 expression; fibroblast-secreted CLDN11 promotes gastric cancer cell proliferation and peritoneal metastasis in vitro and in vivo. Single-cell RNA sequencing, Western blot, immunohistochemistry, in vitro proliferation/migration assays, in vivo peritoneal metastasis model International immunopharmacology Low 38335659
2026 CLDN11 knockdown in rat chondrocytes transcriptionally suppresses Tspan5 expression, leading to attenuation of Notch signaling and acceleration of osteoarthritis cartilage degeneration; Notch pathway inhibitor intervention worsened OA, consistent with CLDN11→Tspan5→Notch as a protective axis. Cldn11 RNAi lentivirus intra-articular injection in rat OA model, Notch inhibitor treatment, qRT-PCR, Western blot, immunohistochemistry, von Frey pain threshold Journal of orthopaedic surgery and research Low 41485015
2024 Cldn11 knockout in mice impairs Sertoli cell polarization and disrupts basal localization of stem cell factor (SCF), a key molecule for spermatogonial maintenance, resulting in impaired differentiating spermatogonial proliferation. Spermatogenesis defects in Cldn11-null mice were not rescued on a severely immunodeficient background, indicating the defect is not caused by autoimmune attack on spermatogenic cells. Autoantibodies against spermatocyte/spermatid antigens were detected in Cldn11-null sera, providing direct evidence that Sertoli cell TJs form an immunological barrier. Cldn11 knockout mouse, immunodeficient background cross (genetic epistasis), serum autoantibody detection, SCF immunolocalization, spermatogonial proliferation assay bioRxivpreprint Medium bio_10.1101_2024.07.16.602181

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 CNS myelin and sertoli cell tight junction strands are absent in Osp/claudin-11 null mice. Cell 587 10612400
1999 Claudin-11/OSP-based tight junctions of myelin sheaths in brain and Sertoli cells in testis. The Journal of cell biology 363 10225958
2001 OSP/claudin-11 forms a complex with a novel member of the tetraspanin super family and beta1 integrin and regulates proliferation and migration of oligodendrocytes. The Journal of cell biology 153 11309411
1992 Heterogeneity of outer membrane proteins in Borrelia burgdorferi: comparison of osp operons of three isolates of different geographic origins. Infection and immunity 127 1563773
1991 OSP: a computer program for choosing PCR and DNA sequencing primers. PCR methods and applications 112 1842929
1999 Access of antibody or trypsin to an integral outer membrane protein (P66) of Borrelia burgdorferi is hindered by Osp lipoproteins. Infection and immunity 108 10338494
1997 Immunization with outer surface protein (Osp) A, but not OspC, provides cross-protection of mice challenged with North American isolates of Borrelia burgdorferi. The Journal of infectious diseases 94 9203661
1995 Borrelia burgdorferi mutant lacking Osp: biological and immunological characterization. Infection and immunity 92 7890424
1997 Borrelia burgdorferi strain-specific Osp C-mediated immunity in mice. Infection and immunity 90 9353047
1991 Molecular mapping of Osp-A mediated immunity against Borrelia burgdorferi, the agent of Lyme disease. Journal of immunology (Baltimore, Md. : 1950) 87 1716290
1993 Variability of osp genes and gene products among species of Lyme disease spirochetes. Infection and immunity 70 8500899
2000 Involvement of OSP/claudin-11 in oligodendrocyte membrane interactions: role in biology and disease. Journal of neuroscience research 57 10700007
1997 Oligodendrocyte-specific protein (OSP) is a major component of CNS myelin. Journal of neuroscience research 57 9418959
2015 A Cholera Conjugate Vaccine Containing O-specific Polysaccharide (OSP) of V. cholerae O1 Inaba and Recombinant Fragment of Tetanus Toxin Heavy Chain (OSP:rTTHc) Induces Serum, Memory and Lamina Proprial Responses against OSP and Is Protective in Mice. PLoS neglected tropical diseases 55 26154421
2000 Developmental expression of OSP/claudin-11. Journal of neuroscience research 46 10797530
2002 Encephalitogenic and immunogenic potential of myelin-associated glycoprotein (MAG), oligodendrocyte-specific glycoprotein (OSP) and 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) in ABH and SJL mice. Journal of neuroimmunology 43 11777540
2005 Disrupted compaction of CNS myelin in an OSP/Claudin-11 and PLP/DM20 double knockout mouse. Molecular and cellular neurosciences 40 15886014
2018 Plasma and memory B cell responses targeting O-specific polysaccharide (OSP) are associated with protection against Vibrio cholerae O1 infection among household contacts of cholera patients in Bangladesh. PLoS neglected tropical diseases 39 29684006
2006 K+ channel KV3.1 associates with OSP/claudin-11 and regulates oligodendrocyte development. American journal of physiology. Cell physiology 37 16624990
2021 MALAT1 Maintains the Intestinal Mucosal Homeostasis in Crohn's Disease via the miR-146b-5p-CLDN11/NUMB Pathway. Journal of Crohn's & colitis 36 33677577
1993 Inability of truncated recombinant Osp A proteins to elicit protective immunity to Borrelia burgdorferi in mice. Journal of immunology (Baltimore, Md. : 1950) 33 8335917
1995 Protection of dogs from Lyme disease with a vaccine containing outer surface protein (Osp) A, OspB, and the saponin adjuvant QS21. The Journal of infectious diseases 29 7706788
2018 Inactivation of the tight junction gene CLDN11 by aberrant hypermethylation modulates tubulins polymerization and promotes cell migration in nasopharyngeal carcinoma. Journal of experimental & clinical cancer research : CR 28 29747653
2021 De novo stop-loss variants in CLDN11 cause hypomyelinating leukodystrophy. Brain : a journal of neurology 26 33313762
2020 lncRNA PCAT18 inhibits proliferation, migration and invasion of gastric cancer cells through miR-135b suppression to promote CLDN11 expression. Life sciences 25 32119960
2019 Disruption of the ovarian serine protease (Osp) gene causes female sterility in Bombyx mori and Spodoptera litura. Pest management science 20 31595658
2017 Bm-muted, orthologous to mouse muted and encoding a subunit of the BLOC-1 complex, is responsible for the otm translucent mutation of the silkworm Bombyx mori. Gene 20 28768207
2005 Effect of saccharide length on the immunogenicity of neoglycoconjugates from synthetic fragments of the O-SP of Vibrio cholerae O1, serotype Ogawa. Carbohydrate research 20 16098493
2007 OSP/claudin-11-induced EAE in mice is mediated by pathogenic T cells primarily governed by OSP192Y residue of major encephalitogenic region OSP179-207. European journal of immunology 18 17549734
2021 MiR-205 suppressed the malignant behaviors of breast cancer cells by targeting CLDN11 via modulation of the epithelial-to-mesenchymal transition. Aging 16 33971623
2004 Borrelia burgdorferi outer surface protein (osp) B expression independent of ospA. Microbial pathogenesis 16 15194158
2012 Transgene-mediated rescue of spermatogenesis in Cldn11-null mice. Biology of reproduction 15 22378758
2019 Induction of systemic, mucosal and memory antibody responses targeting Vibrio cholerae O1 O-specific polysaccharide (OSP) in adults following oral vaccination with an oral killed whole cell cholera vaccine in Bangladesh. PLoS neglected tropical diseases 14 31369553
1996 Experimental immunization against Lyme borreliosis with recombinant Osp proteins: an overview. Infection 14 8740122
2021 An inducible Cldn11-CreERT2 mouse line for selective targeting of lymphatic valves. Genesis (New York, N.Y. : 2000) 13 34338433
2021 Comparative analysis of antibody responses to outer surface protein (Osp)A and OspC in dogs vaccinated with Lyme disease vaccines. Veterinary journal (London, England : 1997) 11 34148599
2006 OSP-Immunofluorescent remyelinating oligodendrocytes in the brainstem of toxically-demyelinated Wistar rats. Arquivos de neuro-psiquiatria 11 16791363
1993 Expression and secretion of outer surface protein (OSP-A) of Borrelia burgdorferi from Escherichia coli. FEMS microbiology letters 9 8339919
2021 Parenteral Vaccination with a Cholera Conjugate Vaccine Boosts Vibriocidal and Anti-OSP Responses in Mice Previously Immunized with an Oral Cholera Vaccine. The American journal of tropical medicine and hygiene 8 33872211
2008 Activation and control of pathogenic T cells in OSP/claudin-11-induced EAE in SJL/J mice are dominated by their focused recognition of a single epitopic residue (OSP58M). International immunology 8 18801757
2024 Unveiling the oncogenic role of CLDN11-secreting fibroblasts in gastric cancer peritoneal metastasis through single-cell sequencing and experimental approaches. International immunopharmacology 6 38335659
2025 The role of CLDN11 in promotion of granulosa cell proliferation in polycystic ovary syndrome via activation of the PI3K-AKT signalling pathway. Scientific reports 5 39875531
1996 Presence of common antigenic epitope in outer surface protein (Osp) A and OspB of Japanese isolates identified as Borrelia garinii. Microbiology and immunology 5 8839432
2025 OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress. Nature communications 4 39746999
2025 Disrupting of IGF2BP3-stabilized CLDN11 mRNA by TNF-α increases intestinal permeability in obesity-related severe acute pancreatitis. Molecular medicine (Cambridge, Mass.) 4 39856555
2024 CCL21 and CLDN11 Are Key Driving Factors of Lymph Node Metastasis in Gastric Cancer. Cancer control : journal of the Moffitt Cancer Center 3 38553809
2024 Ginger inhibits the invasion of ovarian cancer cells SKOV3 through CLDN7, CLDN11 and CD274 m6A methylation modifications. BMC complementary medicine and therapies 2 38575994
2014 Thinking outside the Osp(G)--kinase activation by E2-ubiquitin. The EMBO journal 2 24480478
2010 Protection of CHO cells by transfer of survivin driven by ovarian-specific promoter OSP-2. Molecular biology reports 2 21080083
2024 Limited O-specific polysaccharide (OSP)-specific functional antibody responses in young children with Shigella infection in Bangladesh. bioRxiv : the preprint server for biology 1 39345393
2022 Shigella "Osp"pression of innate immunity. Cell 1 35750030
2026 Cldn11 deficiency aggravates osteoarthritis by inhibiting Notch signalling in a Tspan5-dependent manner. Journal of orthopaedic surgery and research 0 41485015
2026 Generation of an isogenic human induced pluripotent stem cell line harbouring a CLDN11 mutation associated with hypomyelinating leukodystrophy. Stem cell research 0 41932029
2024 CLDN11 deficiency upregulates FOXM1 to facilitate breast tumor progression through hedgehog signaling pathway. Journal of molecular histology 0 39438406
2021 Correction: Plasma and memory B cell responses targeting O-specific polysaccharide (OSP) are associated with protection against Vibrio cholerae O1 infection among household contacts of cholera patients in Bangladesh. PLoS neglected tropical diseases 0 34280200

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