CLDN11 antibody - C-terminal region (ARP33628_P050)
- Known as:
- CLDN11 (anti-) - C-terminal region (ARP33628_P050)
- Catalog number:
- arp33628_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CLDN11 antibody - C-terminal region (ARP33628_P050)
Related genes to: CLDN11 antibody - C-terminal region (ARP33628_P050)
- Gene:
- CLDN11 NIH gene
- Name:
- claudin 11
- Previous symbol:
- OTM
- Synonyms:
- OSP
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-13
- Date modifiied:
- 2016-10-05
Related products to: CLDN11 antibody - C-terminal region (ARP33628_P050)
Related articles to: CLDN11 antibody - C-terminal region (ARP33628_P050)
- Stoploss mutations in CLDN11 were first described as the cause of hypomyelinating leukodystrophy 22 (HLD22). Since then, a novel variant in CLDN11, namely NM_005602.5:c.564del; p.(Arg189ValfsTer31), has been identified in patients with hypomyelinating leukodystrophy resembling HLD22. To better characterize the functional significance of this novel variant and to study the mechanisms underlying CLDN11-related HLDs, isogenic human induced pluripotent stem cell lines carrying the c.564del variant were generated on a PGP1 cell line background. - Source: PubMed
Publication date: 2026/03/28
Gjervan Sophia CSequiera Glen LesterFeng JiaOzgoren OguzVan Belois KatherineKersey BradenRoss ColinKlein Geltink RamonStockler SylviaPouladi Mahmoud A - Male infertility often results from impaired interactions between germ cells and Sertoli cells. While in vitro fertilization and intracytoplasmic sperm injection are widely used, their success depends on the presence of haploid germ cells. Gene therapy remains challenging due to concerns about germline transmission. The mRNA offers a safer option, as its short-life reduces this risk. Here, we show that mRNA delivery into mouse testes restores fertility in a genetic model of infertility. Injected mRNA was specifically expressed in Sertoli cells; although it triggered an innate immune response, spermatogenesis resumed without major side effects. Delivery of naked Cldn11 mRNA into Cldn11-deficient mice, which have meiotic defects due to defective blood-testis barrier, allowed progression from spermatocytes to spermatids. Fertile offspring with normal imprinting were produced via microinsemination. These findings demonstrate the potential of mRNA-based therapy for treating male infertility by targeting testicular somatic cells, without introducing genetic material into the germline. - Source: PubMed
Publication date: 2026/03/05
Kanatsu-Shinohara MitoOgonuki NarumiMatoba ShogoMiyazaki TakehiroMorimoto HirokoLiu TianjiaoYoshinaga NaotoOgura AtsuoUchida SatoshiShinohara Takashi - Hypomyelinating leukodystrophies (HLDs) are a group of hereditary CNS disorders characterized by hypomyelination and, sometimes, repeated cycles of demyelination and remyelination. In HLDs, various genetic mutations in the responsible genes disrupt the morphogenesis of oligodendrocytes (oligodendroglial cells), which wrap neuronal axons with their differentiated myelin sheaths. A stop-loss mutation (c.622T-C or c.622T-G) in the gene encoding claudin family tetraspan plasma membrane protein claudin-11 (CLDN11) is associated with HLD22, which is characterized by incomplete differentiation and hypomyelination or delayed myelination in the brain. Herein, we describe for the first time that a CLDN11 mutant protein with an additional amino acid sequence due to the stop-loss mutation, but not the wild-type protein, leads to decreased expression of oligodendroglial differentiation marker proteins in the FBD-102b oligodendroglial progenitor cell line, the model undergoing its differentiation, at both the molecular and morphological levels. Consistently, mutant exhibited decreased morphological differentiation with a reduced ability to extend processes. These cells contained punctate structures that were partially localized in the endoplasmic reticulum (ER) and stimulated phosphorylation of c-Jun N-terminal kinase (JNK) and eukaryotic translation initiation factor 2A (eIF2A) kinase, ER stress-responsible kinases. Hesperetin, a neuroprotective flavonoid that can downregulate ER stress, recovered the differentiation abilities of these cells. Notably, the effects were related to decreased phosphorylation of ER stress-responsible kinases. JNK was found to be present in a co-precipitate with the hesperetin core, whereby hesperetin inhibited signaling through c-Jun as a negative regulator of differentiation. These findings indicate that the HLD22-associated mutant protein can cause an ER stress response, decreasing cell morphological differentiation. In addition, this study offers possible therapeutic implications for the as-yet-unexplored mechanisms involved in HLD22, at least at the molecular and cellular levels. - Source: PubMed
Publication date: 2026/02/18
Miyamoto YukiOmata TakeruMuraki YutaYagi MoeriYamamoto MasahiroNishi AkinoriYako HidejiYamauchi Junji - Following the downregulation of testicular endocrine and germinative function by slow-release gonadotropin-releasing hormone (GnRH)-agonist implants, testicular functions are quickly restored after implant removal. As an intact blood-testis barrier (BTB) is crucial for normal spermatogenesis and its integrity is FSH- and androgen-dependent, alterations in the BTB gene and protein expressions during downregulation and subsequent restart seem inevitable. We investigated (), () , , and () mRNA-, and CLDN11 and CX43 protein expressions during GnRH implant-induced downregulation (W0) and restart of spermatogenesis after implant removal (week, W, 3-12). Untreated juvenile (JG) and adult dogs (CG) served as controls. Sertoli cells were significantly affected by treatment (reduced nuclear area, , and expressions). All investigated genes (except ) differed significantly during restart (W0-12) compared with CG ( < 0.05). CLDN11 and CX43 immunopositive staining was absent or diffuse cytoplasmic at downregulation and relocated at W9, indicating disruption and subsequent restorage of BTB. As W0 and JG differed considerably, our results suggest that the model cannot mimic puberty. In conclusion, GnRH implant-induced long-term gonadotropin suppression disrupts testicular CX43 and CLDN11 distribution and changes gap and tight junction mRNA expression. Treatment effects are reversible suggesting re-establishment of the BTB. - Source: PubMed
Publication date: 2026/01/14
Goericke-Pesch SandraRöhrs LenaWallrabenstein SvenFrimødt Rønnow AgneteFietz DanielaBrehm RalphLangeheine MarionWehrend AxelHoffmann BerndKörber HannaPackeiser Eva-Maria - This study utilized a novel Proximity Barcoding Assay to perform high-resolution proteomic profiling of individual plasma extracellular vesicles from 85 patients with advanced high-grade serous ovarian carcinoma (OC) and 95 healthy controls (HC). Single-EV analysis identified 119 differentially expressed proteins and 17 distinct EV subpopulations. Cluster 7 (enriched in integrins ITGB3, ITGB1, and ITGA6) was significantly elevated in OC plasma (4.47% in HC vs. 14.79-15.82% in OC). Machine learning (SVM-RFE, LASSO, Random Forest) identified a diagnostic panel (ITGA6, ITGB2, ILK) achieving exceptional accuracy in distinguishing OC from HC (AUC = 0.999 training; 1.000 validation). Furthermore, risk models incorporating specific protein signatures effectively stratified patients by platinum sensitivity/resistance (9-protein panel: ILK, CDCP1, CD86, CLDN4, CLEC1B, CDHR5, CLDN11, JAM2, FOLH1), lymph node metastasis status (7-protein panel: APOE, CD28, CLDN4, FOLH1, ITGAL, JAML, ULBP3), and post-surgical residual disease burden (4-protein panel: CD44, CLMP, ITGA4, AMIGO1), with Cluster 13 (ITGB1-high) also significantly associated with residual disease. This work demonstrates the power of single-EV proteomics combined with machine learning for non-invasive diagnosis and clinical outcome assessment in advanced ovarian cancer, though the absence of early-stage patients limits its applicability for early detection. - Source: PubMed
Publication date: 2026/01/21
Wu BeierYang XupingCai YanlingWan ShihanLiu JingfangXing JieChen XinZhang JiejieJin YanluYu AijunYang Li