PRDX2_RAT Prdx2 ELISA tesk kit
- Known as:
- PRDX2_RAT Prdx2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15081
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- PRDX2_RAT Prdx2 ELISA tesk kit
Ask about this productRelated genes to: PRDX2_RAT Prdx2 ELISA tesk kit
- Gene:
- PRDX2 NIH gene
- Name:
- peroxiredoxin 2
- Previous symbol:
- TDPX1
- Synonyms:
- PRP, NKEFB, TSA, PRXII, PRX2, MGC4104
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-07-06
- Date modifiied:
- 2016-10-05
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- The oviduct provides an optimal environment to protect gametes and embryos against oxidative stress, yet its endogenous defenses remain insufficiently characterized. This study examined the expression and the spatial, temporal and hormonal regulation of four major antioxidant enzyme families - peroxiredoxins (PRDX), catalase (CAT), superoxide dismutases (SOD), and glutathione peroxidases (GPX) - in the bovine oviduct. Oviducts from cyclic cows were analyzed in three complementary experiments. In vivo (Experiment 1), mRNA expression of antioxidant enzymes (CAT, GPX1-3, PRDX1-6, SOD1-2) was compared between oviductal regions (ampulla vs. isthmus) and estrous cycle stages (pre-ovulatory, post-ovulatory, luteal). In vitro (Experiment 2), physiological concentrations of progesterone (100 ng/mL) and estradiol (300 pg/mL) were tested on gene expression in ampullary and isthmic epithelial spheroids. In Experiment 3, GPX protein abundance and enzymatic activity were assessed in oviductal fluid. All transcripts were detected in the oviduct epithelium. GPX1-3 and PRDX6 showed region-specific expression, with GPX1-2 enriched in the ampulla and GPX3 and PRDX6 in the isthmus. Stage-dependent variations were observed for CAT, SOD2, PRDX2, PRDX4, and PRDX6 in a region-dependent manner. Progesterone upregulated GPX2 and PRDX6 in both ampullary and isthmic spheroids, while estradiol selectively stimulated PRDX4 expression in isthmic spheroids. GPX3 protein abundance decreased at the post-ovulatory stage, in both regions, and mirrored the GPX activity in the oviduct fluid. These results demonstrate that antioxidant enzyme expression in the bovine oviduct is dynamically regulated by region, cycle stage, and hormonal milieu, highlighting their role in maintaining redox homeostasis during early reproductive events. - Source: PubMed
Publication date: 2026/09/23
Braga Rachel FerreiraMaia Ana Lucia Rosa E SilvaPereira Paulo Victor Dos SantosDouet CécileCarvalho Anaïs VitorinoMermillod PascalDemattei Marie-VéroniqueSouza-Fabjan Joanna Maria GonçalvesSaint-Dizier Marie - Glioblastoma multiforme (GBM) exhibits strong resistance to radiotherapy, partly driven by glioblastoma stem-like cells (GSCs) with enhanced redox homeostasis and DNA repair capacity. This study evaluated whether targeting Nrf2-mediated antioxidant signaling and PARP1-dependent DNA repair enhances GSC radiosensitivity to different radiation modalities. Pharmacological inhibition of Nrf2 (ML385, 6 µmol/L) or PARP1 (olaparib, 5 µmol/L) reduced tumorsphere formation to 74.5 ± 10% and 58.56 ± 14.5% of control levels, respectively, while combined treatment further reduced formation to 51 ± 11% and sphere size to 29% of control. Western blotting confirmed effective pathway inhibition, with complete suppression of PARP activity and approximately 30% reduction in Nrf2 downstream proteins (SOD1, PRDX2, and NQO1). Dose-response analysis showed D₅₀ values of 5.03 ± 0.09 Gy (photons), 2.96 ± 0.91 Gy (protons), and 2.04 ± 0.47 Gy (carbon ions), corresponding to RBE₅₀ values of 1, 1.70 ± 0.55, and 2.46 ± 0.57, respectively. ML385 enhanced radiosensitivity to photons and protons and showed a similar radiosensitizing trend following carbon-ion irradiation, whereas olaparib showed its strongest effect with photons and limited effects with protons and carbon ions. Combined treatment produced a greater reduction in radiation survival than either inhibitor alone under selected conditions, particularly following photon irradiation. Nrf2 inhibition reduced downstream antioxidant proteins and increased late apoptotic/necrotic fraction, while PARP1 inhibition was associated with altered DNA damage persistence. Combined inhibition further increased γ-H2AX foci at selected time points following proton irradiation, consistent with delayed or incomplete repair of radiation-induced DNA damage. These findings support Nrf2 and PARP1 as potential regulators of GSC radioresistance and provide a rationale for further investigation of their therapeutic targeting in combination with radiotherapy. - Source: PubMed
Publication date: 2026/09/05
Salma RimaHammad MiraHariri MehranSangsuwan TraimateMoloudi KaveScherthan HarryVela AnthonyCesário RuteGodoy PauloBalosso JacquesStenerlöw BoHaghdoost Siamak - Intracerebral hemorrhage (ICH) remains the most severe stroke subtype with high mortality and disability rates. Although apigenin has shown cerebroprotective potential in preclinical studies, its mechanism of action, particularly in hypertensive ICH, remains poorly understood. This study investigates the molecular pathway through which apigenin confers protection against hypertensive ICH. We employed a hypertensive ICH mouse model treated with varying apigenin doses. Through transcriptomic profiling, molecular docking, surface plasmon resonance (SPR), and pull-down assay, we identified peroxiredoxin 2 (PRDX2) as a direct target of apigenin. Prdx2 mice and recombinant human thioredoxin 1 (rhTrx1) rescue experiments were utilized to validate the signaling pathway. Histological analysis, western blot, immunofluorescence, and zymography were applied to assess hemorrhage, oxidative stress, inflammation, and extracellular matrix (ECM) remodeling. Apigenin administration significantly reduced ICH incidence, hemorrhage volume, and area while enhancing vascular integrity, independent of blood pressure changes. We identified PRDX2 as a direct binding partner of apigenin, with their interaction stabilizing PRDX2 expression. PRDX2 deficiency abolished apigenin's protective effects and exacerbated oxidative stress, neuroinflammation, and vascular damage. Furthermore, apigenin upregulated Trx1 expression via PRDX2, and rhTrx1 administration rescued the protective phenotype in Prdx2 mice by reducing oxidative damage, inflammatory cell infiltration, and vascular smooth muscle cell apoptosis. Our study elucidates a novel apigenin-PRDX2-Trx1 antioxidant signaling pathway that protects against hypertensive ICH through blood pressure-independent mechanisms. These findings not only provide a mechanistic foundation for developing apigenin-based therapeutics for cerebrovascular diseases, but also offer novel strategies and entry points for future clinical translation. - Source: PubMed
Publication date: 2026/09/01
Xu Hao-ChenLiu MingSun Ying-YingPing Jie-DanCui Qing-HuaChen Jing-ZhouLi Hao - Uterine receptivity is critical for successful embryo implantation, yet epithelial-specific proteomic changes during this transition remain incompletely characterized. This study aimed to profile changes in protein expression in isolated mouse endometrial epithelial cells between the pre-receptive (Day 1) and receptive (Day 4) phases of pregnancy to identify key pathways associated with uterine receptivity. - Source: PubMed
Publication date: 2026/07/06
Jitjumnong JakreeInyawilert WilasineeTiantong AttapolWang Shih-HanChen Chao-JungLiao Yu-JingMoonmanee TossapolHuang San-YuanTang Pin-Chi - Cholangiocarcinoma (CCA) is a major complication of primary sclerosing cholangitis (PSC), with a 20-year incidence of ∼15%. Early detection is challenging, as current surveillance rarely identifies CCA at a resectable stage. This study investigated bile-derived extracellular vesicles (EVs) as a liquid biopsy source for protein biomarkers enabling early diagnosis and prediction of CCA in PSC. - Source: PubMed
Publication date: 2026/08/21
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