PON2
- Known as:
- PON2
- Catalog number:
- Y214456
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PON2
Related genes to: PON2
- 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
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- 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 - A plethora of studies have demonstrated the pathophysiological roles played by paraxonase 2 (PON2) in oxidative stress control, inhibition of apoptosis, infections, and the progression of various types of malignancies. The continuous interest in PON2 has not gone hand in hand with the development of its inhibitors. Indeed, only one inhibitor for PON2, namely TQ416, is known, although neither its preparation nor a systematic structure-activity relationship analysis has been so far reported. Herein, we outline the first study aimed at the definition of structure-activity relationships of TQ416 by the preparation of a small library of its analogues. Successfully, we identified some [1,2,4]triazolo[4,3-]quinoline derivatives more potent than TQ416 as PON2 inhibitors, and among them one endowed with an IC value in the nanomolar range. We tested the parent TQ416 and its most effective congener in cells showing their effectiveness and complex behaviour. - Source: PubMed
Publication date: 2026/03/26
Bianconi ElisaLampitella Eros AntonioNigro FatimaRossi LudovicaZambri FedericoFava SimoneMarone MariaPorzio ElenaMacchiarulo AntonioManco GiuseppeMarinozzi Maura - : Long-term exposure to polychlorinated biphenyls (PCBs), including the mixture of PCBs in Aroclor1260 (Ar1260), results in metabolic dysfunction-associated steatotic liver disease (MASLD) in mice and humans. While the effects of PCBs on gene expression are well-documented using short-read RNA sequencing, the regulatory roles of alternative splicing (AS) and differential transcript usage (DTU) are uncharacterized. AS has been implicated in MASLD. Previously, we reported that chronic (34 wks.) exposure of normal, low-fat-diet (LFD)-fed male mice to Ar1260 resulted in 12 hepatic RNA modifications. Proteomic analysis of these same liver samples identified Ar1260 exposure-associated changes in selenoproteins: GPX4 and SELENBP2 were increased and SELENOS and SELENOF were reduced. : Here we used long-read isoform sequencing (IsoSeq) to identify DTU in four genes in the Ar1260-exposed livers: , , , and . : Network analysis of the corresponding proteins revealed a strong association with pathways relevant to MASLD including lipid metabolism, glycolysis, and oxidative stress. : These findings suggest that PCB exposure alters the transcript isoform landscape of key metabolic genes involved in MASLD. - Source: PubMed
Publication date: 2026/01/25
Petri Belinda JPiell Kellianne MWahlang BanridaChariker Julia HRouchka Eric CCave Matthew CKlinge Carolyn M