AQP3_BOVIN AQP3 ELISA tesk kit
- Known as:
- AQP3_BOVIN AQP3 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen8450
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- EIAab
- Gene target:
- AQP3_BOVIN AQP3 ELISA tesk kit
Related genes to: AQP3_BOVIN AQP3 ELISA tesk kit
- 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
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- Breast cancer remains a leading cause of global mortality in women, with therapy resistance posing a major challenge to successful treatment. Chemotherapy-induced oxidative stress can trigger adaptive survival mechanisms through the antioxidative transcription factor NRF2 and membrane pores known as peroxiporins. Peroxiporins regulate cellular redox homeostasis by controlling the flux of H2O2, potentially driving the development of chemoresistance in aggressive subtypes. This study investigated the expression of peroxiporins, AQP3 and AQP5, and the antioxidative transcription factor NRF2, before and after chemotherapy to determine their role in chemotherapy resistance in HER2-positive and triple negative breast cancer. - Source: PubMed
Publication date: 2026/08/10
Guteša IlijaBubanovic SandaVodopic TonciMlinaric MonikaGrgat KrešimirCipak Gašparovic Ana - The exposure to ultraviolet (UV) radiation is one of the key exogenous processes that contribute to photoaging, oxidative stress, and barrier dysfunction. Naematelia aurantialba is a very rare medicinal and edible fungus which is an organism with a large pharmacological potential, yet there is a gap in understanding the molecular processes involved in the anti-photoaging and soothing repair actions that the fermentation product is known to possess. The aim of this study was to understand the protective role of Naematelia aurantialba fermentation broth (NAF) against UV-induced skin cells damage and the possible molecular mechanisms of damage. The fermentation of Lactobacillus plantarum was used to prepare NAF. Its physicochemical characteristics were measured by use of DPPH, hydroxyl radical scavenging, and elastase inhibition and its biocompatibility by use of erythrocyte hemolysis experiment. We created UVA induced HFF-1 photoaging model, UVB induced HaCaT barrier damage model, and capsaicin induced sensitive model in order to measure cell viability and expression of factors associated with them. It was found that NAF had a large free radical scavenging capacity and elastase activity, and had a great biocompatibility over its interesting concentration (hemolysis rate < 5%). Molecularly, NAF activates mitochondrial homeostasis, boosting the gene and protein expression of the SIRT1 and SIRT3 proteins, and thereby strongly prevents the release of the enzyme, matrix metalloproteinase-1 (MMP-1) and suppressed collagenase degradation. At the same time, NAF prevents the capsaicin-induced overexpression of TRPV1 substantially preventing neurogenic inflammation, and increases aquaporin 3 (AQP3) and claudin-1 (CLDN1), mending the skin barrier. The NAF can produce various anti-photoaging, soothing, and barrier repair effects by activating the dermal SIRT1/3- MMP -1 axis, and blocking the epidermal TRP V1 pathway, which justifies its potential as an innovative functional plant raw material. - Source: PubMed
Publication date: 2026/08/04
Yuan QinxuanChen YanShi DoudouYou ShiquanCui MimiLiang DongjieWang ChangtaoLi Meng - To investigate the transcriptional profiling of ocular surface ectoderm (OSE) derived from human embryonic stem cells (hESC), and identified CACNG6 and AQP3 as the surface markers of OSE. - Source: PubMed
Publication date: 2026/08/18
Sun LuLi Yu-MingSong Yu-WenYang Yi-ChenDuan LianGao YangLi Jian-XinYu Yan-KunPang Kun-PengDang Guang-FuZhang Can-Wei - Inflammation is a primary driver of skin ageing. Mussel mucin, a naturally occurring anti-inflammatory protein, suffers from inefficient extraction from its natural source. To overcome the yield limitation of natural sources and to verify the biological activity of the recombinant protein, this study employed synthetic biology techniques to efficiently produce and purify the recombinant mussel mucin Mfp151 and subsequently evaluated its anti-inflammatory and skin barrier repair functions. Using human immortalized keratinocytes (HaCaT), human foreskin fibroblasts (HFF-1), and human monocyte leukemia cells (THP-1) as models, we assessed the skin-repairing, antioxidant, and anti-inflammatory effects of Mfp151 the CCK-8 assay, qPCR, transmembrane resistance measurement, scratch assay, ELISA, and free radical scavenging assays. In vivo validation was conducted with a zebrafish sunburn model. The results demonstrated that Mfp151 significantly promoted cell proliferation (80 μg/mL treatment increased HaCaT cell proliferation by approximately 32%) and migration, while upregulating the expression of key skin barrier genes , , and by 2.14-3.88 folds. Mfp151 effectively scavenged DPPH and ABTS free radicals while enhancing cellular antioxidant capacity by activating the Nrf2 pathway. Regarding anti-inflammatory effects, Mfp151 significantly suppressed lipopolysaccharide-induced production of pro-inflammatory factors IL-6, TNF-α, and IL-1β (80 μg/mL treatment reduced expression levels to 59.87%-79.12% of that in the model group), while significantly downregulating the expression of key inflammatory mediators COX-2 and iNOS and their downstream product PGE2 (80 μg/mL treatment reduced , expression and PGE2 secretion to 48.91%-67.30% those in the model group.) Zebrafish experiments confirmed the significant promotion of Mfp151 on caudal fin repair following sunburn. The data indicate that the recombinant Mfp151 obtained through synthetic biology techniques possesses skin-repairing functions alongside antioxidant and anti-inflammatory activities, thus demonstrating promising application prospects in fields such as anti-ageing cosmetic ingredients and wound dressings. - Source: PubMed
Zhang ChaoLi QuanfeiPan LiangWang YuFang MingyuanShao ZhengyangChen QianHe KundongLei PengGu Yi'anSun LiangZhan YijingLu QianjinXu HongWang Rui - Dry eye disease (DED) is a multifactorial ocular surface disorder characterized by inflammation, oxidative stress, tear film instability, and secretory dysfunction. This study investigated the protective effects of Lute-gen, a lutein and zeaxanthin-based formulation, in both in vitro and in vivo DED models. Human corneal epithelial (HCE-T) cells were stimulated with TNF-α, while dry eye was induced in female Sprague-Dawley rats using subcutaneous scopolamine (SCP) administration. In HCE-T cells, Lute-gen showed no cytotoxicity, restored cell viability, reduced intracellular ROS, and was associated with increased expression of antioxidant-related markers (Nrf2, HO-1, SOD, CAT, and GPx), reduced expression of inflammatory mediators (TLR4/MyD88/NF-κB/NLRP3), and increased expression of AQP3 and AQP5. In SCP-induced rats, Lute-gen significantly improved tear secretion and reduced corneal fluorescein staining. Histopathological analyses revealed restoration of conjunctival goblet cells, mucin staining, corneal epithelial integrity, acinar area and cell density, and lacrimal gland architecture, with reduced inflammatory infiltration. Immunofluorescence further demonstrated reduced TLR4 and MMP9 immunoreactivity and decreased CD68 inflammatory cell infiltration. Molecular analyses showed reduced expression of inflammatory cytokines and NF-κB/MAPK/MMP signaling-related inflammatory mediators, together with restoration of AQP1, AQP3, and AQP5 expression in corneal tissues. Collectively, these findings suggest that Lute-gen treatment was associated with improvements in dry eye-related pathological changes, including restoration of antioxidant-related markers, attenuation of inflammatory responses, restoration of aquaporin expression, and preservation of ocular surface and lacrimal gland integrity. These preclinical findings support further mechanistic investigations and the future clinical evaluation of Lute-gen as a potential nutritional intervention for dry eye disease. - Source: PubMed
Publication date: 2026/07/13
Sood RachitSanjay Lee Hae-Jeung