Ask about this productRelated genes to: PON1 Blocking Peptide
- Gene:
- PON1 NIH gene
- Name:
- paraoxonase 1
- Previous symbol:
- PON
- Synonyms:
- ESA
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: PON1 Blocking Peptide
Related articles to: PON1 Blocking Peptide
- Apolipoprotein A1 (APOA1) and paraoxonase 1 (PON1) are key proteins of high-density lipoproteins (HDL). The aim of the present study was to obtain and characterize an in vitro model for endogenous APOA1 and PON1 longstanding upregulation in hepatocytes that can be further used to decipher the mechanisms of their protective action. Cultured human hepatocytes (HuH-7 cell line) were transfected with CRISPR/dCas9 activation plasmids targeting / genes. Following selection with specific antibiotics, RNA sequencing was used for the transcriptomic characterization of the transfected hepatocytes. The functionality of the secreted APOA1/PON1 was evaluated as the capacity of the conditioned medium (CM) from transfected HuH-7 to modulate the oxidative and inflammatory stress in TNFα-activated primary human umbilical endothelial cells (HUVEC). The results showed that: (1) a robust, longstanding upregulation (46 days) of endogenous / was obtained after CRISPR/dCas9 transfection and antibiotics selection; (2) / upregulation led to a modified transcriptomic profile and increased the expression of several antioxidant genes in transfected hepatocytes as demonstrated by RNAseq analysis; (3) secreted APOA1/PON1 were functional as demonstrated by the CM ability to reduce the levels of reactive oxygen species and inflammatory markers (VCAM-1, MCP-1) in TNFα-activated HUVEC. In conclusion, we achieved an experimental model of successful longstanding upregulation of endogenous APOA1 and PON1 in human hepatocytes. The targeted proteins are secreted in a functional form and can be used for deciphering their complex mechanism of protective action in various pathological conditions. - Source: PubMed
Publication date: 2026/07/02
Haratau Jessica I CNiculescu Loredan SBarbalata TeodoraSanda Gabriela MFuior Elena VSasson ShlomoSima Anca VStancu Camelia SToma Laura - Paraoxonases (PONs) are a family of three isozymes, PON1, PON2, and PON3, with lactonase and esterase enzymatic activities. These enzymes have been implicated in the pathophysiology of numerous disorders, including cancer, atherosclerosis, liver diseases, neurodegenerative conditions, and toxicities. Specifically, alterations in PONs, such as changes in gene expression, mRNA levels, protein abundance, and enzymatic activity, have been associated with a range of pathological conditions. PONs are primarily linked to these disorders through their antioxidant and detoxifying functions, although additional, yet unidentified, mechanisms may also contribute. A growing body of evidence indicates that modulating PON levels or activity of PONs may confer therapeutic benefit in the prevention, management, and treatment of certain diseases. Promising strategies include enzyme replacement therapy, drug repurposing, and genetic engineering techniques aimed at restoring or enhancing PON function. Moreover, PONs' level and activity can be influenced by life-style factors and the microbiome, offering additional avenues for intervention. In this review, we propose that the modulation of PONs holds therapeutic and preventive potential, and we discuss the current and emerging strategies by which this may be achieved. - Source: PubMed
Publication date: 2026/07/14
Tehrani Fateh SepandTehrani Fateh SahandZiai Seyed Ali - The genetic background of hypertriglyceridemia is complex. In this systematic review and meta-analysis, we determined genetic variants associated with fasting triglyceride (TG) and very-low-density lipoprotein-TG (VLDL-TG) concentrations in European adults. - Source: PubMed
Publication date: 2026/06/29
Nuwaylati Dena AMensink Ronald PJoris Peter JCoort Susan L MPlat Jogchum - Maternal obesity has been associated with an increased risk of oxidative and metabolic disorders in offspring later in life. This study investigates the therapeutic effects of -acetylcysteine (NAC), a potent antioxidant, on obesity-induced inflammation, oxidative stress and impaired glucose metabolism in an experimental rat model. Maternal obesity was induced in female rats by administering a high-fat diet (HFD) (60% kcal from fat). NAC was given via intragastric gavage at a dose of 150 mg/kg. Female rats were mated at 12 weeks of age, and the respective diets were maintained throughout gestation and lactation. The experiment was concluded on postnatal day 28, at which point the offspring's blood samples and liver tissues were collected for analysis. Following standard histological processing, immunohistochemical staining was performed to detect oxidative markers in liver tissue sections. In the HFD + NAC group, NAC supplementation ameliorated histological damage in both mothers and offspring's liver tissues. NAC treatment reduced 8-OHdG expression in the HFD + NAC group, indicating a protective effect against oxidative stress. NAC also had a modulatory effect on oxidative stress markers such as total oxidant status, oxidative stress index, PON1, ARES and malondialdehyde. HFD induces hepatic injury and oxidative stress in both dams and their offspring, contributing to impaired metabolic programming. Maternal NAC supplementation partially ameliorated these effects by reducing oxidative damage and improving glucose metabolism. However, its protective effects were limited, particularly in restoring antioxidant enzyme activity and fully normalizing metabolic parameters. - Source: PubMed
Publication date: 2026/07/13
Tatar TugbaTüfekci Kıymet KübraTatar Musa - Risk stratification in hepatocellular carcinoma (HCC) is limited by the lack of robust biomarkers reflecting tumor biology. The antioxidant enzyme Paraoxonase-1 (PON1) shows prognostic potential, yet its role in tumor tissues and the feasibility of non-invasive assessment remain unclear. - Source: PubMed
Publication date: 2026/07/10
Cai ChiyuHao YuqiXue YushuLi DongxiaoWang YikeYue XinyuHou JunjingWang ZipengLi Bing YaoXie MengZhuang HaoLi DeyuDing Xiangming