PON2 polyclonal antibody
- Known as:
- PON2 pab (anti-)
- Catalog number:
- PAB18578
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PON2 polyclonal antibody
Related genes to: PON2 polyclonal antibody
- Gene:
- PON2 NIH gene
- Name:
- paraoxonase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-25
- Date modifiied:
- 2014-11-19
Related products to: PON2 polyclonal antibody
Related articles to: PON2 polyclonal antibody
- Paraoxonase 2 (PON2) is an enzyme exhibiting both lactonase and esterase activities, widely distributed across various tissues and localized within cellular mitochondria. It plays a vital role in innate immunity by restricting bacterial infections and has diverse functions, including the regulation of mitochondrial reactive oxygen species levels and the management of endoplasmic reticulum stress. By alleviating oxidative stress, stabilizing mitochondria, and modulating apoptosis, PON2 emerges as a significant factor in the study of cellular senescence. This review consolidates recent findings regarding PON2's physiological roles, its mechanistic connections to senescence, and the therapeutic potential of modulating its activity. Our analysis highlights PON2's considerable promise as a target for aging-related diseases, including neurodegeneration, metabolic disorders, cardiovascular diseases, chronic inflammation, and cancer. - Source: PubMed
Publication date: 2026/04/29
Kim Hyeong HwanKang Ye JinLee Jae HoLee Hyeong MinPark Hyung SoonNam Chang-Hoon - BACKGROUND: Retinoblastoma is a pediatric intraocular cancer usually driven by RB1 gene mutations, with Y79 cells serving as a retinoblastoma model bearing RB1 inactivation. Paraoxonases (PON1, PON2, PON3) are antioxidant proteins; PON1 is HDL-associated, whereas PON2 and PON3 are intracellular, with PON2 localized to the inner mitochondrial membrane. The PI3K/Akt pathway is a key survival cascade frequently hyperactivated in cancer. This study evaluated PON isoform expression in Y79 retinoblastoma cells and examined whether their regulation is mediated by PI3K/Akt signaling. METHODS: Adult Retinal Pigment Epithelial (ARPE-19), Human Retinal Endothelial Cells (HREC), Human Retinal Pericytes (HRP), and Y79 cells were cultured under standard conditions, serum-starved, and treated with the Akt pathway inhibitor LY294002 (5 & 10 µM). Gene expression was assessed using quantitative real-time PCR. Protein expression of Akt, phosphorylated Akt (p-Akt), and PON2 was analyzed by Western blotting. Statistical analyses were performed using one-way ANOVA, and data were expressed as mean ± SEM. RESULTS: Our results showed that the expression of PON1 was increased; PON2 and PON3 were decreased in Y79 cells when compared with HREC, and ARPE-19. The expression of p-Akt was elevated in Y79 cells, and LY294002 decreased the expression of p-Akt and PON1 and PON3 without altering PON2 mRNA expression, indicating that there is differential regulation of PON genes in Y79 cells and is regulated by the PI3K/Akt pathway. CONCLUSION: These findings indicate that PI3K/Akt signaling sustains a pro-survival, antioxidant phenotype in retinoblastoma cells through selective regulation of PON isoforms, highlighting this pathway as a promising therapeutic target. - Source: PubMed
Publication date: 2026/04/17
Ravi RamyaShajahan SathikSuresh Babu JayavigneeswariBharathi Devi S R - This study aims to explore the potential molecular mechanisms by which di (2-ethylhexyl) phthalate (DEHP) exposure induces pulmonary arterial hypertension (PAH). - Source: PubMed
Publication date: 2026/03/20
Li HuaJiang YingchunLi Jijia - Chemotherapy-induced peripheral neuropathy (CIPN) is a prevalent and debilitating adverse effect associated with the use of different anticancer drugs such as platinum compounds, taxanes, vinca alkaloids, and proteasome inhibitors. In the current experimental study, we investigate the neuroprotective effects of umbelliferone against oxaliplatin (OXA)-induced peripheral neuropathy in rats. Intraperitoneal administration of OXA (4 mg/kg) was used for induction of neurotoxicity in the rats. The rats subsequently received the oral administration of umbelliferone at a dose of 2.5, 5, and 10 mg/kg. The mechanical withdrawal threshold (MWT), cold allodynia testing, nerve conduction activity, body weight, cerebrum weight, cerebrum index, acetylcholinesterase (AchE), total protein, nitric oxide (NO), antioxidant, inflammatory cytokines, apoptosis, and inflammatory parameters were estimated. The different mRNA expressions were measured in the brain tissue. Umbelliferone treatment improved the MWT and reduced the cold allodynia. Umbelliferone significantly (P < 0.001) improved the nerve conduction velocity, along with the body weight, cerebrum weight, cerebrum index, and altered the levels of acetylcholinesterase (AchE), total protein, and nitric oxide (NO). Umbelliferone treatment altered the level of antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), malonaldehyde (MDA)); inflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), IL-10, IL-18); inflammatory parameters (cyclooxygenase-2 (COX-2), inducible nitric oxide synthetase (iNOS), prostaglandin E (PGE), nuclear factor kappa B (NF-κB)); apoptosis parameters (caspase-3, caspase-9, Bcl-2 Associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), Bax/Bcl-2 ratio). Umbelliferone treatment altered the mRNA expression paraoxonase (PON)-1, PON-2, PON-3, and peroxisome proliferator-activated receptor δ (PPAR-δ). The findings clearly showed the neuroprotective effect of umbelliferone against OXA-induced neurotoxicity in rats via alteration of NF-κB, PPAR-δ, and mitochondrial apoptosis pathways. - Source: PubMed
Publication date: 2026/03/27
Li XiaohuiHan YuTian HanCheng ZihuiZuo JingjingShen Qingxia - The sodium-hydrogen exchanger-1 (NHE1) is a ubiquitously expressed transmembrane transporter that plays a central role in maintaining intracellular pH homeostasis and supporting normal cellular function. In cancer, NHE1 is overexpressed in many tumor types and has been associated with increased cancer cell metastasis and proliferation. Beyond these established roles, emerging evidence implicates NHE1 as a regulator of cancer cell metabolism. By driving intracellular alkalinization and shaping the tumor microenvironment, NHE1 influences metabolic pathway activity, mitochondrial function, redox balance, and cellular stress responses. In this review, we synthesize current evidence linking NHE1 dysregulation to metabolic reprogramming in cancer, with a focus on mitochondrial metabolism, glycolytic flux, lysosomal biology, and reactive oxygen species-associated stress pathways. We further evaluate pharmacological strategies targeting NHE1, emphasizing their metabolic consequences, translational potential, and the challenges that have limited clinical application to date. Collectively, this review highlights NHE1 as a potential integrator of ion transport and metabolic control in cancer and discusses how targeting NHE1-driven metabolic programs may support the development of novel therapeutic strategies. - Source: PubMed
Publication date: 2026/03/15
Al-Hamaly Majd AForester Beau RBlackburn Jessica S