PON2 antibody
- Known as:
- PON2 (anti-)
- Catalog number:
- orb73691
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- PON2 antibody
Related genes to: PON2 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 antibody
Related articles to: PON2 antibody
- : To date there is a lack of an integrative review literature on redox homeostasis, oxidative stress and the influence on metabolic pathways and plasticity in uveal melanoma (UM), since most literature findings are from cutaneous melanoma (CM), a genetically and behaviorally distinct cancer. Furthermore, UM metabolic pathway comparison to other cancers could provide more insight into metastatic UM, a difficult-to-treat malignancy. : A wide-ranging multi-step literature search of PubMed and Web of Science for redox balance, oxidative stress, antioxidants and metabolic plasticity in UM, with expanded search terms for connections with other cancers. : UM cells maintain redox homeostasis via several redox loops: glutathione, thioredoxin, peroxiredoxins, peroxisomal catalase and the mitochondrial antioxidative network. NADPH plays a key role in regenerating UM antioxidative capabilities. Key redox signaling pathways are the subject of ongoing research in UM: NRF2 signaling, AMPK, mTOR, MAPK, FoxO. These pathways are less studied versus CM and present behavior differences in UM. PON2, studied in CM, represents a literature gap in UM. Inside the tumoral microenvironment, UM presents high metabolic plasticity and easy switching from glycolysis to oxidative phosphorylation (OXPHOS). Thus, UM eschews the classic Warburg effect loop and instead presents high oxidative phosphorylation (OXPHOS) gene expression, which generates additional lactate, which in turn produces cascade reprogramming in the metabolic pathways and lactate metabolism particularities associated in experimental studies with immune-escape phenomena. Uveal melanoma's OXPHOS capabilities confer survival advantages and subdivide tumoral populations into OXPHOS-high and OXPHOS-low variants. Glycolysis/OXPHOS metabolic plasticity is an ongoing research field in other cancers with common and different elements vs. UM: cutaneous melanoma, small cell lung carcinoma, pancreatic cancer, breast cancer, acute myeloid leukemia, prostate cancer, renal cell carcinoma and glioblastoma. Uveal melanoma cells are susceptible to deleterious effects of prooxidants, a metabolic vulnerability which helps to create genetic pleomorphism, selecting higher proliferation and dissemination variants. : Uveal melanoma is an oncogenic mutation and mitochondrial metabolism-driven malignancy, with metabolic connections to other malignancies. Emerging understanding of redox homeostasis, redox pathway signaling, mitochondrial oxidative and oncogenic metabolism could lead to better understanding of therapeutic response and new therapeutic targets. This review novelly integrates the general and CM redox literature with the UM literature, painting a complex redox signaling and metabolic plasticity picture of UM. - Source: PubMed
Publication date: 2026/07/25
Păsărică Mihai AdrianCurcă Paul FilipDragosloveanu Christiana Diana MariaNisipașu Cosmin IonuțCurcă George Cristian - Osteosarcoma (OS) is the most common bone cancer, known for its aggressive nature, high chemoresistance, and strong metastatic potential responsible for poor clinical outcomes. In this context, identifying reliable biomarkers and therapeutic targets is therefore critical. This study investigates the role of paraoxonase-2 (PON2), an intracellular enzyme known for its anti-oxidative and anti-apoptotic properties. PON2 overexpression has been observed in various cancers and is implicated in tumor development and progression. - Source: PubMed
Publication date: 2026/08/03
Gerini EleonoraPompei VeronicaCecati MoniaCampagna RobertoPozzi ValentinaFilosa AlessandraGoteri GaiaSalvolini EleonoraEmanuelli MonicaSartini Davide - 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 - Genetic, epigenetic, and transcriptomic analyses have stratified medulloblastoma (MB) into four canonical subgroups of Wingless Type (WNT), Sonic Hedgehog (SHH), and Group 3 and Group 4, with distinct patient profiles and prognoses. Recent classification strategies have also considered combining Group 3 and Group 4 tumors into a Non-WNT/Non-SHH subgroup to account for biological overlap and heterogeneity. Using high-dimensional gene expression data from 487 pediatric and young adult patients and over twenty-one thousand transcripts, this study explores which genes can improve prognostic accuracy for survival while accounting for molecular stratification, histological subtype, key oncogenic drivers (MYC and MYCN amplification), and established clinical covariates, including age group (< 3 vs. 3-21 years) and metastatic status. We then develop a multi-stage framework for identifying prognostic genes and evaluating modern survival modeling strategies. In the first stage, gene screening was performed using Benjamini-Hochberg adjusted Cox regression across false discovery rate (FDR) thresholds from 1% to 6%, with the number of retained genes increasing from 15 at 1% to 146 at 6% FDR. In the second stage, multiple survival models were evaluated, including LASSO, Elastic Net, Ridge regression, SCAD, MCP, PCA-Cox, and Random Survival Forests, using ten-fold cross-validation with the Integrated Brier Score as the primary calibration metric and the concordance index as a secondary discrimination measure. Although Ridge regression achieved the lowest prediction error at higher FDR thresholds, it did not perform variable selection and retained large gene sets, limiting interpretability. In contrast, the 6% FDR Elastic Net model provided an optimal balance between predictive accuracy and model sparsity while reducing the gene set from 146 to 49 genes, yielding an interpretable final multivariable model. Gene-level effects from the final Elastic Net-penalized Cox model revealed a clear prognostic gradient. Genes associated with poorer survival included FKBP4, CSNK2A2, GPC4, GATA3, NPY, LYPD1, CLCA4, and BNC2, which have been implicated in tumor progression, signaling pathways, and immune-related processes, whereas genes associated with improved survival included ZNF774, COX10, FBLIM1, and UNC13C, reflecting roles in cellular regulation and protective biological processes. These findings demonstrate that combining FDR-based screening with Elastic Net-penalized Cox modeling yields a robust, parsimonious, and biologically meaningful prognostic framework for medulloblastoma, achieving strong predictive performance while maintaining interpretability in high-dimensional genomic settings. - Source: PubMed
Publication date: 2026/07/01
Amona Elizabeth BSumy Mst Sharmin AkterJones TylerWang ShuoyangMistry Akshitkumar MRaj AshokDonninger HowardYaddanapudi KavithaKong Maiying - Proliferative diabetic retinopathy (PDR) is one of the leading causes of blindness in working-age adults. We have previously shown that the risk of PDR is significantly elevated in individuals with intrauterine exposure to famine. However, the genetic mechanisms mediating this association remain unknown. The aim of the current study was to investigate the molecular underpinnings of famine-related PDR by performing genome-wide association (GWAS) and interaction studies (GWIS). - Source: PubMed
Publication date: 2026/06/25
Fedotkina OlenaBegum Most ChampaTrinh Xuan TungÖzgumus TurkulerÅkerlund MikaelNilsson PeterSpindola Leticia MariaLyssenko Valeriya