AQP3
- Known as:
- AQP3
- Catalog number:
- 001807A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AQP3
Related genes to: AQP3
- 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
Related articles to: AQP3
- Chronic exposure to inorganic arsenic affects more than 200 million people, and disease outcome varies widely among individuals with comparable intake. Explanations have centered on arsenic metabolism, which acts on arsenite that is already inside the cell. Uptake sits upstream of metabolism and sets how much arsenite reaches the genome, yet whether it acts as a gene-by-environment modifier of genotoxicity has been asserted far more often than it has been measured. We expressed human aquaporin-3 (AQP3), its point mutants and the paralogues AQP7, AQP9 and AQP10 in three human cell lines, and measured DNA damage as γH2AX by flow cytometry against a damage threshold re-derived from mock-transfected cells in every experiment. In lung fibroblasts, AQP3 raised the γH2AX-high fraction 2.36-fold at 5 μM arsenite. Because a gene-by-environment interaction widens the genotype gap with dose while an independent genotoxin would not, the combination exceeds what the two factors would produce if they simply added by 6.36 percentage points, which is an interaction. The response required the AQP3 sequence, was suppressed by N-acetylcysteine in proportion to arsenite dose, was absent in RKO cells, and was shared with AQP9 and AQP10, which created an arsenite dose-response in a cell line that had none of its own. Low-input RNA sequencing of 135 ten-cell pools located the effect inside the cell: at an identical 1 μM applied dose and within a single batch, AQP3 raised (induced when trivalent arsenic modifies KEAP1 thiols, and so a report of intracellular rather than applied exposure) 3.3-fold, a shift equivalent to 40% of the 1-to-10 μM interval on the measured dose-response, while AQP3 without arsenite was indistinguishable from untreated. Duplex sequencing detected no consistent change in somatic mutation frequency from arsenite alone at any dose to 10 μM, in an assay that resolved a 26-fold response to N-ethyl-N-nitrosourea; the arsenite-induced mutation frequency at the locus nonetheless differed 1.61-fold by AQP3 genotype. The interaction is therefore not unique to AQP3, and aquaglyceroporin complement belongs alongside metabolism among the host factors that set arsenic susceptibility. - Source: PubMed
Publication date: 2026/09/24
Yin ShiweiFeng BingruVaziripour MaryamSlewitzke Shannon EFernandes Gail FYun JihyeAmos Christopher IXia Jun - Human metabolism converts inorganic arsenic to the pentavalent methylated species MMA(V) and DMA(V), the forms most people excrete, and the forms long read as the end of a detoxification pathway. Whether a transporter sets how much of these metabolites reaches the genome has not been tested in a mammalian cell. We expressed human AQP3, AQP7, AQP9 or AQP10 in HEK293T and MRC5-SV40 cells and measured γH2AX by flow cytometry across dose series of As(V), MMA(V) and DMA(V), pairing every aquaporin with a GFP-Tubulin control and an untransfected mock acquired in the same run. As(V) was inactive in HEK293T cells and only weakly active in MRC5-SV40 cells to 20 µM, and both methylated species damaged DNA only in the millimolar range, DMA(V) being the more potent of the two in both cell lines. Against that weak baseline, AQP9 and AQP10 raised DMA(V)-induced γH2AX in HEK293T cells by roughly 17 percentage points over the matched control, more than doubling the damage the same exposure produced in control cells, whereas AQP3 and AQP7 changed it not at all. AQP9 alone remained active with MMA(V). The ranking held in MRC5-SV40 fibroblasts at one-sixth the size, and within single wells the damage rose with the amount of AQP9 a cell carried while the control was flat. Aquaglyceroporins therefore discriminate among arsenic species, and AQP9 and AQP10 turn a weakly genotoxic metabolite into a substantially more genotoxic one. - Source: PubMed
Publication date: 2026/09/25
Yin ShiweiFeng BingruVaziripour MaryamXia Jun - 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