Cldn23
- Known as:
- Cldn23
- Catalog number:
- 039893A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Cldn23
Related genes to: Cldn23
- Gene:
- CLDN23 NIH gene
- Name:
- claudin 23
- Previous symbol:
- -
- Synonyms:
- CLDNL
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-14
- Date modifiied:
- 2016-10-25
Related products to: Cldn23
Related articles to: Cldn23
- Future long-duration human space missions will expose astronauts to chronically reduced gravitational loading, a condition associated with oxidative stress and epithelial barrier dysfunction. The intestinal epithelial barrier depends on tight junctions (TJs), yet the impact of partial gravity on TJ composition, assembly, and claudin organization remains poorly defined. Here, we show that differentiated intestinal epithelial monolayers exposed to simulated Mars gravity undergo TJ ultrastructural remodeling, characterized by loss of apical membrane "kissing points" and widening of the paracellular space, accompanied by impaired barrier function. Simulated Mars gravity also induces oxidative stress and accumulation of cytoplasmic and nuclear lipid droplets, consistent with altered membrane and lipid homeostasis. At the molecular level, simulated Mars gravity promotes selective TJ changes, with significant downregulation-but not mislocalization-of barrier-forming claudins CLDN1 and CLDN3 and the scaffolding protein ZO-1, while CLDN2, CLDN4, CLDN7, CLDN12, CLDN23, and OCLN remain unchanged. STAT3 activation, but not ERK or NF-κB signaling, may be associated with these alterations and is consistent with a stress-adaptive remodeling response to oxidative stress under simulated Mars gravity. Overall, these findings identify simulated Mars gravity as a disruptor of intestinal barrier homeostasis and highlight TJ remodeling as a target for countermeasures to preserve gut integrity during deep-space missions. - Source: PubMed
Publication date: 2026/05/18
Benvenuti LauraBertini ChiaraMarcelli GemmaIppolito ChiaraCiti ValentinaGiovannoni RobertoIacopetti PaolaGambino GaetanaRossi LeonardoAngeloni DeboraManzoni DiegoSalvetti Alessandra - Presently, we investigated hypothesized roles and mechanisms of cell type-specific, selective activation of different vascular NOX (NADPH oxidase) isoforms in obesity and metabolic syndrome. - Source: PubMed
Publication date: 2026/04/23
Huang KaiHuang YuanliZhang YuhanZhang YixuanHatch Nicholas WFreed Julie KCai Hua - Colorectal cancer (CRC) progression involves complex mechanisms of invasion and metastasis. Claudin-2 (), a tight junction protein, has emerged as a key regulator paracellular permeability and its dysregulation is implicated in chronic inflammatory diseases and cancer. The present study aimed to determine the mechanisms by which deletion affects genes associated with motility and invasion of colon cancer cells. CRISPR/Cas9 was used to knock out in HCT116 cells. Subsequently, gene expression was analyzed using reverse transcription-quantitative PCR and migratory capacity was assessed using wound healing assays. deletion led to the downregulation of genes associated with motility and metastasis, including zonula occludens-1-associated nucleic acid binding protein, N-Myc downstream-regulated gene 1, and , suggesting that supports pro-migratory gene networks. These findings demonstrated that regulates metastatic gene expression in CRC. Although further mechanistic studies are warranted, the present study provided notable genetic and phenotypic evidence of the role of in promoting cancer cell migration and invasion, offering a potential foundation for future studies into its signaling interactions and therapeutic potential. - Source: PubMed
Publication date: 2025/11/27
Alghamdi Rana AAl-Zahrani Maryam H - Laryngeal cancer is a prevalent and aggressive type of head and neck malignancy that often presents with a poor prognosis. Its high incidence and significant mortality rate pose a substantial challenge in clinical management, but the prognostic biomarkers and the mechanisms of progression are poorly understood. We sought to identify the prognostic biomarkers and their effects in the progression of laryngeal cancer. - Source: PubMed
Publication date: 2025/10/22
Huang ShaokunShan XuanSong FanWu MinLi ChaofanWang XiaohuiZhao RuipingYe Juan - Ulcerative colitis (UC) is a chronic inflammatory condition marked by immune dysfunction and disruption of the intestinal epithelial barrier, in which mast cells play a significant role through the release of inflammatory mediators. Recent advances suggest that mast cell-derived exosomes and intraluminal vesicles (MC-EXOs and MC-ILVs) may contribute to disease pathogenesis by modulating epithelial tight junction proteins, particularly members of the Claudin family. Notably, transcriptomic analyses indicate that CLDN23, a gene encoding Claudin-23, is downregulated in active UC. Exosomes are emerging as key players in intercellular communication, capable of delivering functional microRNAs and proteins that influence intestinal permeability and immune cell behaviour. This mini-review summarizes current evidence on the interaction between mast cell-derived vesicles and intestinal epithelial cells, focusing on their regulatory role in Claudin expression and immune signalling pathways. Understanding these mechanisms may inform the development of exosome-based biomarkers and therapeutic strategies for UC. - Source: PubMed
Publication date: 2025/09/10
Li Shao-HanXu Hao-MingHuang Hong-LiZhou Yong-Jian