Ask about this productRelated genes to: PON3 antibody
- Gene:
- PON3 NIH gene
- Name:
- paraoxonase 3
- 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: PON3 antibody
Related articles to: PON3 antibody
- The intrauterine environment strongly influences children's health and development. Distinct cardiovascular biomarkers have been linked to birth weight and later weight gain, with correlations observed in maternal and umbilical cord serum. - Source: PubMed
Publication date: 2026/03/07
Kabbani NouraEbert ThomasStepan HolgerLia MassimilianoBlüher MatthiasBaber RonnyVogel MandyBiemann RonaldKiess WielandTönjes AnkeSchrey-Petersen Susanne - Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder shaped by genetic variants and network-level interactions beyond obesity and insulin resistance. This study aimed to define the genetic and proteomic architecture of MASLD by integrating GWAS and plasma proteomic profiling from the UK Biobank. Genome-wide association analyses were conducted under additive and dominant models, with functional annotations performed using SIFT, PolyPhen-2, PROVEAN, REVEL, CADD, MutationTaster, and conservation metrics (GERP++, phyloP, phastCons, and B-statistic). Differential protein expression was assessed using the Olink platform, and STRING was applied for protein-protein interaction analysis. MASLD patients showed male predominance and significant differences in hepatic (AST, ALT, GGT, PDFF), metabolic (glucose, triglycerides, TyG index), and inflammatory markers (CRP, neutrophils, NLR, CAR). GWAS confirmed (rs738409, I148M) and (rs58542926, E167K) as major risk variants, while and showed weaker but conserved associations. Proteomics revealed downregulation of IGFBP2, IGFBP1, PON3, CKB, and APOF and upregulation of CPM, IGSF9, GUSB, ACY1, AFM, LEP, and GSTA1/3. PPI analysis identified ADIPOQ, LEP, FGF21, and ADH1B as central hubs in metabolic and inflammatory regulation. MASLD should be regarded as a network disease involving lipid metabolism, insulin/IGF signaling, mitochondrial function, and ECM-inflammatory pathways. These findings highlight and as major genetic drivers, while , , and peripheral proteins contribute regulatory roles, suggesting novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/28
Kang Sang WookKim Su KangBan Ju YeonPark Min Su - Persistent symptoms following SARS-CoV-2 infection are the hallmark of post-COVID condition (PCC), also referred to as long COVID. However, the underlying molecular mechanisms remain poorly understood. In this study, we employed data-independent acquisition mass spectrometry (DIA-MS)-based plasma proteomics to identify molecular alterations associated with PCC. DIA-MS proteomic analysis revealed a clear distinction between the plasma proteome of uninfected individuals and those previously infected with SARS-CoV-2, irrespective of PCC status. PCC samples demonstrated downregulation of the antioxidant protein peroxiredoxin 6 (PRDX6) and upregulation of oxidative stress-associated proteins, particularly vanin-1 (VNN1) and paraoxonase-3 (PON3). Additionally, individuals with PCC exhibited significantly elevated levels of six proteins-PCSK9, CST3, C1Q, CPB2, KNG1, and GAPDH-associated with glycolysis, complement and coagulation cascades, and inflammatory pathways. Validation by ELISA does not necessarily reflect the proteomics data suggesting the requirement for alternate methods of validation. Nonetheless, oxidative stress, as measured by 8-hydroxy-2'-deoxyguanosine (8-OHdG), further showed that PCC samples had significantly higher levels of DNA damage, compared with convalescent individuals. Antioxidant markers, including reduced and oxidized glutathione (GSH and GSSG), were significantly lower in PCC samples than in uninfected controls. Collectively, these findings indicate that plasma proteomic alterations persist for at least 3 months following SARS-CoV-2 infection, with additional disruptions in oxidative stress and inflammatory pathways characterizing individuals with PCC. - Source: PubMed
Publication date: 2026/04/17
Chowdhury Mohammad Mobarak HQuenum Akouavi Julite IrmineRioux-Perreault ChristineLucier Jean-FrançoisIlangumaran SubburajPiché AlainAllard-Chamard HuguesRamanathan Sheela - 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 - 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