Ask about this productRelated genes to: RAI14 antibody
- Gene:
- RAI14 NIH gene
- Name:
- retinoic acid induced 14
- Previous symbol:
- -
- Synonyms:
- NORPEG, KIAA1334, RAI13, DKFZp564G013
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-20
- Date modifiied:
- 2016-10-05
Related products to: RAI14 antibody
Related articles to: RAI14 antibody
- Oral lichen planus (OLP), a chronic inflammatory disease affecting the stratified squamous epithelium of oral mucosa (mucositis), presents treatment challenges due to rapid washout of conventional topical gels. This study developed prednisolone acetate-loaded mucoadhesive electrospun nanofibers using PVP K90/Eudragit RS100 via Super ES-3 technology to enhance drug retention and therapeutic efficacy. Nanofibers exhibited uniform morphology (diameter ranging from185 ± 0.3 nm to 704 ± 0.3 nm), neutral surface pH (7.4 ± 0.1), and superior mucoadhesion of 0.03N and bond strength of 0.455 Nmm. FTIR confirmed polymer-drug compatibility and XRD studies revealed crystalline state of drug in nanofibers. In vitro release from prednisolone acetate-loaded nanofibers followed zero-order kinetics (r = 0.999, RMSE = 1.02%, 90.21% Q₁₂ₕ), ideal for sustained delivery vis a vis. prednisolone acetate dispersion that followed Korsmeyer-Peppas model (r = 0.962, RMSE = 3.99, 51.34% Q). In vivo evaluations using 4% SDS-induced mucosal irritation model in Wistar rats shown irritation score of 4.333 ± 0.58 in disease control, nanofibers achieved near-complete resolution (score 1.000 ± 0.58, equivalent to vehicle p = 0.7538), significantly outperforming marketed formulation (3.000 ± 0.58, p = 0.0015; using one-way ANOVA F = 45.2, p < 0.0001). Histopathology confirmed superiority with no signs of irritation or tissue damage of the oral mucosa showing normalized rete ridges and minimal inflammation. These findings demonstrate mucoadhesive nanofibers as a promising localized delivery system for OLP, providing sustained prednisolone acetate release, prolonged buccal retention of 7 h, and superior therapeutic outcomes while minimizing systemic corticosteroid exposure. - Source: PubMed
Publication date: 2026/03/16
Sachin Dhaliwal Jagjit SinghKaur Amanpreet - Reduced levels of circulating gonadal hormones in post-menopausal women can negatively affect various physiological functions, including brain and gut deficits. There is an urgent need to find novel strategies to mitigate estrogen-gut-microbiome-brain axis (EGMBA) dysfunction. This study aimed to investigate the effect of fructooligosaccharide (FOS), a non-digestible prebiotic fiber, on estrogen deficiency-induced alterations in the EGMBA using an ovariectomized (OVX) rat model. Adult female SD rats were bilaterally OVX to induce estrogen deficiency and associated EGMBA dysfunction. Rats were administered FOS (50 mg kg p.o.) for 28 consecutive days. To assess EGMBA dysfunction, after 28 days, we performed behavioral tests, biochemical estimations (oxidative stress), molecular estimations (inflammatory markers ELISA), gene expression analysis (HPA axis, monoamine neurotransmission, apoptosis, gut microbiota alterations, & gut barrier integrity RT-PCR/qPCR), and histopathological analysis. Administration of FOS significantly improved behavioral outcomes (reducing anxiety and depression, and improving memory). FOS also attenuates oxidative stress and inflammatory markers. FOS regulates apoptosis (upregulation of and downregulation of ), HPA axis functioning (corticosterone, , , & ), and monoamine neurotransmission ( & ) in the hippocampus of OVX rats. FOS also promoted healthy cell growth and prevented apoptosis. Additionally, FOS restored gut microbial eubiosis, improved mucus secretion (), preserved tight junction protein expression (, , & ), and maintained the colon microstructure. FOS exerts multifaceted protective effects on the EGMBA by modulating gut and brain functions. These findings support its potential as a non-hormonal therapeutic approach for managing postmenopausal complications. - Source: PubMed
Publication date: 2026/03/09
Chaudhary RishabhBansal NitinLal RoshanKaur AmanpreetBishnoi MahendraKondepudi Kanthi KiranChopra KanwaljitBansal Seema - To evaluate the inhibitory effect of antitumor component-Ι in venom (AHVAC-I) on proliferation and migration of cisplatin-resistant gastric cancer cells and explore the underlying mechanism. - Source: PubMed
Li YanyuLi Cheng Dai ChuanjunGuo RunzhiHan HaoyuLu LinmingZhou FangfangZhi Hui支 慧 - Macrophage antigen presentation is crucial for adaptive immunity and maintaining immune balance, including anti-infection, anti-tumor, and inflammation regulation. However, its role in tumor immunomodulation is less understood compared to macrophage polarization. This study explored how Rnaseh2c macrophages influence hepatocellular carcinoma (HCC) progression using in vitro cell models and mouse tumor models. Single-cell RNA sequencing, immunoblotting, immunofluorescence, immunoprecipitation, and flow cytometry analysis were employed to examine RNASEH2C's impact on macrophage antigen presentation. Our results indicated that Rnaseh2c macrophages, which were non-polarized, promoted HCC growth by inhibiting antigen presentation. RNASEH2C facilitated lysosomal degradation of RAI14 by enhancing TRAF3IP1 expression and suppressing the mTOR pathway, with HSC70 and CMTM6 playing opposing roles in RAI14 degradation. RAI14, a skeleton protein, facilitated the macropinocytosis of MHC II molecules and tumor-associated antigen, thus activating Th1 cells in HCC. In conclusion, our study revealed how RNASEH2C mediated RAI14's lysosomal degradation, offering potential targets and strategies for HCC immunotherapy. - Source: PubMed
Publication date: 2025/12/08
Pan BanglunYu HuahuiLin ZikunLiu MengxinLiu JiayuXu YiqingWu LinqingZhang QiuyuWang Zengbin - Retinoic acid (RA), a metabolite of vitamin A, exerts paradoxical effects in tissue repair, promoting regeneration in some contexts while driving fibrosis in others. However, the mechanisms governing this functional switch remain elusive. Here, we identify RA as a key paracrine signal that links tubular epithelial injury to fibroblast activation in renal fibrosis. Spatial metabolomics and single-cell transcriptomics reveal that ALDH1A2-mediated RA synthesis is upregulated in injured renal tubules, while RA receptor signaling is enriched in interstitial fibroblasts. RA stimulation induces fibroblast-to-myofibroblast transition (FMT) by upregulating RAI14, a cytoskeletal adaptor that binds and stabilizes TRIOBP, thereby preventing its HECTD1-mediated ubiquitination and degradation. This stabilization enhances F-actin assembly and cytoskeletal tension, leading to YAP nuclear translocation and activation of profibrotic transcriptional programs. Genetic ablation of RAI14 significantly attenuates renal fibrosis in vivo. Together, our findings uncover a tubule-derived RA-RAI14-TRIOBP-YAP axis that translates epithelial injury into fibroblast mechanotransduction, providing mechanistic insight into epithelial-mesenchymal communication and a potential therapeutic target for fibrotic kidney disease. - Source: PubMed
Publication date: 2025/11/14
Zhu JunWang MeixiaZhang YizhiWang XintaoDai LeiLi ZhuLi YangbingZhang XinxinWang HongjieZhao JieLi XiaozhouWang Hong-Hui