Ask about this productRelated genes to: AQP3 antibody
- Gene:
- AQP3 NIH gene
- Name:
- aquaporin 3 (Gill blood group)
- Previous symbol:
- -
- Synonyms:
- GIL
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-25
- Date modifiied:
- 2019-04-23
Related products to: AQP3 antibody
Related articles to: AQP3 antibody
- Cheilitis is a lip-specific inflammatory disorder lacking safe long-term therapies. Topical glucocorticoids are limited by adverse effects, highlighting the need for plant-derived immunomodulators with dual anti-inflammatory and barrier-repairing effects. - Source: PubMed
Publication date: 2026/09/28
Zhu AnmingLiu JunxiCao XianxianWu JiahuiXiao FengkunLiu YouyunShen YanzhenWang FeifeiQu Liping - Phyllanthus amarus Schum. & Thonn is a medicinal plant, documented for its folkloric use in the treatment of malaria. This study investigated the antimalarial potential and mechanism of action of bioactive compounds purified from Phyllanthus amarus. Through bioactivity-guided assay, the dichloromethane fraction was obtained from the methanol extracts, and Phyllanthin, Stigmasterol-methyl siaresinolate mixture were purified from it using chromatographic and spectroscopic techniques. Thirty male mice were infected with Plasmodium berghei (ANKA strain) and treated after parasitemia confirmation for five consecutive days. Percentage parasitemia and chemosuppression were determined using microscopy. Host mitochondrial permeability transition (mPT) pore opening, FoF ATPase, and lipid peroxidation were determined using spectrophotometry. Inflammatory cytokines, biomarkers for liver toxicity and some glycolytic enzymes were assessed using ELISA. Gene expressions for mitochondrial complexes, matrix metalloproteinases (MMP2) and MMP9, creatine kinase, and troponins (TnI, TnC, and TnT), Janus kinase (JAK), aquaporin-3 (AQP3), and cGMP were determined. At 10 mg/kg, the Stigmasterol-Methyl siaresinolate mixture had the highest chemo-suppression and the least percentage parasitemia, reversed the mPT pore opening, decreased FoF ATPase activity, and lipid peroxidation. The compounds decreased inflammatory biomarkers, markers for liver toxicity, and modulated glycolytic enzymes. These compounds enhanced mitochondrial complexes, cGMP, and MMP2 and MMP9 expressions while it downregulated the expressions of AQP3, Creatine kinase, TnI, TnC, and TnT, as well as JAK genes. These compounds may have exerted this effect through mitochondrial protection, modulation of metabolic and inflammatory pathways, and regulation of gene expression, supporting their potential as therapeutic candidates for drug-resistant malaria. - Source: PubMed
Publication date: 2026/09/27
Babarinde Cecilia OpeyemiOlanlokun John OludeleBodede OlusolaIdowu Thomas OyebodeSteenkamp Paul Anton - Functional constipation is a common gastrointestinal disorder that impairs quality of life. Although probiotics have shown benefits in constipation, whether live and heat-killed forms of the same strain act through similar mechanisms remains unclear. This study compared the effects of live and heat-killed K56 in experimental constipation. - Source: PubMed
Publication date: 2026/09/12
Zhao ZhiLi XinyiHe JianWang RanLan LianhangHe JingjingGuo JieLi YixuanZhao WenLi Xiaoxia - Glioblastoma (GBM) frequently recurs after temozolomide (TMZ) therapy and exhibits substantial redox plasticity. Our previous work showed that the effects of hydrogen peroxide (HO) vary with its level and between parental and TMZ-resistant GBM cells. Succinate dehydrogenase subunit D (SDHD), a membrane-anchoring component of mitochondrial complex II, is positioned at the interface of electron transport and redox homeostasis, but its regulation in GBM remains unclear. We therefore examined whether SDHD expression changes across distinct HO-responsive contexts involving aquaporins (AQPs) and AKT. TCGA transcriptomic analysis showed higher SDHD mRNA expression in WHO grade IV than in grade II/III gliomas, whereas paired primary/recurrent high-grade glioma samples showed heterogeneous SDHD changes at recurrence. TMZ reduced SDHD, and SDHD knockdown decreased intracellular reactive oxygen species. Combined redox perturbation reduced SDHD, whereas AKT inhibition restored SDHD expression. Under receptor-associated signaling conditions, EGFRvIII expression or CXCL12 stimulation increased measured HO together with AQP3, AKT Ser473 phosphorylation, and SDHD. In TMZ-resistant cells, pharmacological perturbation of aquaporin-associated signaling decreased AQP9 together with AKT Ser473 phosphorylation and SDHD. An AQP3-targeting compound further reduced cell density when combined with TMZ. Together, these findings suggest that changes in SDHD expression are consistent with a compensatory redox response in GBM cells and that its regulation varies with the nature of HO-associated signaling during TMZ-related stress. - Source: PubMed
Publication date: 2026/09/05
Tsai Kuen-JangChen Kuan-TsoTsai Chin-ChuanHong Zi-XuanQiu Li-YingLiu Chan-ChuanChang Kwang-YuChen Pin-YuanChien Chia-Hung - Genome-wide association studies (GWAS) have uncovered multiple loci associated with atopic dermatitis (AD), although mechanistic understanding remains limited. Here, we examine a risk variant in the aquaporin 3 (AQP3) promoter and propose a mechanistic link between genotype to altered autophagy, skin barrier integrity, and wound healing in AD. A GWAS involving 1261 AD cases and 4062 controls of Chinese ancestry from the Singapore-Malaysia cohort was performed. Linkage disequilibrium (LD) analysis and cis-eQTL datasets were used to assess regulatory associations. Functional effects of promoter variants were validated using in vitro luciferase assays and ex vivo transcriptomic profiling. In vitro experiments in HaCaT keratinocytes investigated the effect of siRNA-mediated AQP3 knockdown on autophagy, skin barrier integrity, and wound closure. A discovery GWAS identified significant association between AD and SNP rs12555686 (p = 1.67 × 10, OR = 1.89), located in the promoter of AQP3. Two additional SNPs in strong LD (rs2231225, rs3758279) formed a major haplotype associated with reduced AQP3 expression. Reduced AQP3 expression was associated with decreased autophagy markers (Beclin1, ATG5, ATG12, GABARAPL2, LAMP2, ATG4C), increased senescence markers (p21, GADD45A, SERPINE1), and elevated inflammatory cytokines (IL8, IL1B, TNF). Lastly, AQP3 knockdown in HaCaT keratinocytes reduced steady-state LC3B-II/LC3B-I ratio, reduced occludin expression, and delayed wound healing in vitro. Promoter variants in AQP3 link genetic susceptibility to gene signatures consistent with altered autophagy, cellular senescence, and inflammation in AD. These findings highlight AQP3 as a potential modulator of both epithelial and immune-related mechanisms in AD pathogenesis. - Source: PubMed
Lim Yi Ying ElizaSio Yang YieLam Terence Yin WengSay Yee-HowReginald KavitaChew Fook Tim