CLDN3 (Claudin 3)

No difference was observed in the number of goblet cells between WT and TRPV6KO mice; however, the expression of intercellular junction proteins, including E-cadherin, claudin-3, and occludin, was significantly suppressed in TRPV6KO mice compared with WT mice. These findings suggest that TRPV6 protects against DSS-induced colitis, potentially by regulating epithelial barrier function through intracellular junction protein expressions.

It is concluded that CLDN3 expression is common in lung cancer, that its level of expression is higher in AC than in SCC, and that a reduced expression level is associated with unfavorable outcome in both SCC and AC. Once anti-CLDN3 targeted drugs should prove to be safe and efficient, NSCLC may represent a major application for such treatments.

Our findings indicate that aberrant CP development is a central mechanism underlying post-radiation contrast-enhanced brain lesions, and that an RBE of 2 should be considered when determining dose thresholds for normal tissue tolerance in carbon ion therapy for brain tumors.

Presented results suggest that CLDNs may serve as biomarkers for diagnosis and prognosis as well as therapeutic targets in CNS tumors. Further investigation is essential to clarify their clinical relevance and therapeutic potential.

Microbiome analysis indicated that Bt-CO supplementation increased the diversity of gut microbiota, promoted beneficial microorganisms but suppressed pathogenic microorganisms within the intestines of tilapia. In conclusion, incorporating Bt-CO into the diet at 1 × 108 CFU/g shows significant probiotic potential and effectively enhances tilapia's disease resistance, which is likely attributed to its role in strengthening non-specific immunity and improving fish intestinal health and microecology.

Rescue experiments demonstrated that overexpression of CLDN3 could partly reverse the inhibitory effects of ASCL2 deletion on the malignant capacities of BC cells, suggesting their synergistic effects. Collectively, ASCL2 is a pivotal biomarker for successful individualized cancer therapy, targeting ASCL2 has enormous therapeutic potential.

Our findings indicate that elevated serum claudin-3 levels are associated with MF and correlate with disease severity, suggesting that claudin-3 may serve as a valuable biomarker for monitoring disease progression. Further research is required to elucidate its underlying mechanisms and assess its potential as a therapeutic target in MF.

Additionally, the elevated butyric acid levels in the BELR47-treated group supported its potential to mitigate gut barrier dysfunction and alleviate intestinal inflammation. Therefore, G. vaginalis infection induces inflammation in both the vagina and colon, disrupts the gut microbiome, and alters fecal metabolites, thereby supporting the concept of a "vagina-gut axis."

Our work supports the notion that three overlapping features-low expression of Claudin-3/4/7, high NF-YA long/NF-YA short ratio and a 158-gene signature-mark a specific subset of STAD characterized by mesenchymal features and poor prognosis.

These findings demonstrate that copper-induced intestinal inflammation and pyroptosis are driven by ROS-NLRP3 axis activation, while simultaneously compromising mucosal barrier integrity. This study elucidates critical mechanisms of copper toxicity in broilers and highlights risks associated with excessive copper exposure.

Moreover, BCU inhibited the AKT/NF-κB signal pathway, as indicated by markedly reduced the protein expression of p-NF-κB and p-AKT (p < 0.01). Collectively, the findings suggested that BCU effectively alleviates intestinal damage induced by APEC-infection through AKT/NF-κB signal pathway to modulate oxidative stress and inflammatory response.

Rutin enhances intestinal barrier function and mitigates X-ray-induced barrier disruption by preventing the downregulation of ZO-2, occludin, and claudin-3 at both the mRNA and protein levels, thereby reinforcing epithelial integrity. Rutin may serve as a natural radioprotective agent, preserving gut barrier function during radiation exposure.