Ask about this productRelated genes to: PCYOX1 antibody
- Gene:
- PCYOX1 NIH gene
- Name:
- prenylcysteine oxidase 1
- Previous symbol:
- -
- Synonyms:
- KIAA0908, PCL1
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-25
- Date modifiied:
- 2014-11-19
Related products to: PCYOX1 antibody
Related articles to: PCYOX1 antibody
- Loss of cardiomyocytes during hypoxia-reoxygenation injury contributes to adverse myocardial remodeling, resulting in hypertrophy of surviving cardiomyocytes, interstitial fibrosis, and ultimately, heart dysfunction. Despite extensive research in the field, there is currently no specific treatment available for myocardial hypoxia-reoxygenation injury to prevent cardiomyocyte death. Prenylcysteine oxidase 1 (PCYOX1) is a pro-oxidant, FAD-dependent thioether oxidase that generates hydrogen peroxide during prenylcysteine metabolism, but its role in cardiomyocytes is poorly defined. Here, using HL-1 cardiomyocytes stably silenced for Pcyox1, we show that PCYOX1 contributes to both basal and stress-induced oxidative burden and cell death. Pcyox1 silencing reduced reactive oxygen species (ROS) levels at baseline and blunted the ROS increase during ischaemic/hypoxic stress. Consistently, Pcyox1 silencing decreased apoptosis after prolonged ischaemic/hypoxic exposure. Quantitative proteomics of whole-cell lysates and isolated mitochondria revealed coordinated remodeling of pathways involved in energy buffering and contractile machinery, including increased abundance of mitochondrial creatine kinases (CKMT1/CKMT2), acetyl-CoA synthetase 2-like (ACSS1), and multiple myosin components, changes that persisted under ischaemic/hypoxic stress and after reoxygenation. Overall, these data identify PCYOX1 as a modulator of redox homeostasis and proteomic adaptation in cardiomyocytes and support PCYOX1 inhibition as a potential strategy to limit hypoxia-reoxygenation-associated injury. - Source: PubMed
Banfi CristinaBrocca LisaBascucci AlicePapaianni Giulia GiusyMallia AliceEligini Sonia - Methylprednisolone (mPSL) pulse therapy is an essential treatment for systemic lupus erythematosus (SLE); however, it carries a risk of osteonecrosis of the femoral head (ONFH). The pathogenesis of ONFH involves neutrophil extracellular trap (NET)-mediated microcirculation disorders. In BALB/c mice with imiquimod (IMQ)-induced lupus, mPSL pulse elevated serum levels of prenylcysteine oxidase 1 (PCYOX1), an enzyme that produces NET inducers hydrogen peroxide and farnesal, resulting in increased NETs in vivo. Although ischemia was observed in the femoral head, IMQ + mPSL-treated BALB/c mice did not develop ONFH. PCYOX1 is abundant in very-low-density lipoproteins. This study aimed to demonstrate that hyperlipidemia exacerbates NET-mediated microcirculation disorders and leads to ONFH development following mPSL pulse in lupus mice. To address this, ApoE mutant hyperlipidemic and BALB/c mice with IMQ-induced lupus received mPSL pulse. NET-forming neutrophils in peripheral blood were detected by flow cytometry. ONFH was assessed microscopically. As a result, IMQ + mPSL-treated ApoE mutant but not BALB/c mice developed ONFH, exhibiting higher levels of PCYOX1 and NET-forming neutrophils in circulation. In addition, NET-forming neutrophils accumulated in the vessels surrounding the femoral head, accompanied by osteocyte necrosis. This study demonstrated that mPSL pulse in lupus mice with hyperlipidemia enhanced PCYOX1 levels and NET formation, resulting in ONFH development, suggesting that hyperlipidemia may be a risk factor for ONFH following mPSL pulse therapy in SLE. - Source: PubMed
Publication date: 2026/04/09
Ogawa HodakaOgawa NahoFukuyama MizukiHomma ShotaArai SuishinUchizawa MomoManabe RikuTakai KokiWashio ChinaHori IkumaNishibata YukaMasuda SakikoSakurai ToshihiroHui Shu-PingWatanabe-Kusunoki KanakoNakazawa DaigoTomaru UtanoShimizu TomohiroIwasaki NorimasaIshizu Akihiro - This study utilized Mendelian randomization (MR) to investigate the causal relationship between circulating plasma proteins and lung adenocarcinoma. - Source: PubMed
Publication date: 2025/06/04
Zhang WeiyuanChen NanLi ChangxiSu XitianFu ZhuoZhong YoushuangDeng Huojin - Deep venous thrombosis (DVT) and poor long-term patient outcomes frequently occur in patients with Achilles tendon rupture (ATR). Biomarkers for DVT and their possible relationship to long-term healing outcomes remain unexplored. To identify DVT biomarkers from proteomic profiles during the inflammatory and proliferative healing stages and assess their associations with one-year healing outcomes after surgical repair of ATR. A cohort of 53 patients undergoing standardized ATR repair from previous clinical trials was investigated. Intraoperative inflammatory-stage tendon biopsies were obtained from 40 patients, and tendon microdialysates from 28 patients were collected two weeks later during the proliferative stage. Liquid chromatography-tandem mass spectrometry proteomic profiles were linked to DVT status at two weeks post-surgery using ultrasonography screening and to patient-reported outcomes at one-year post-surgery. Six candidate DVT biomarkers were identified from tendon biopsies, whereof four (ABI3BP, IGKV2-40/IGKV2D-40, PCYOX1, STIP1) were associated with one-year healing outcomes. In tendon microdialysates, 43 candidate DVT biomarkers were identified, but none were associated with healing outcomes. Bioinformatic analysis revealed pathways related to heat shock response, platelet signaling, collagen and extracellular matrix metabolism, and immunoglobulins. The results support shared inflammatory-stage protein pathways in regulating venous thrombosis and reported healing outcomes, where elements of individual hypoxic tolerance and platelet signaling emerge as potential key links. - Source: PubMed
Publication date: 2025/03/01
Saarensilta AnnukkaChen JunyuReitzner Stefan MarkusHart David AAhmed Aisha SAckermann Paul W - It is unknown whether there are differentially expressed proteins (DEPs) in the circulating exosomes of appropriate- vs. small-for-gestational-age (AGA vs. SGA) infants, and if so, whether such DEPs relate to measures of endocrine-metabolic health and body composition in childhood. Proteomic analysis in cord-blood-derived exosomes was performed by label-free quantitative mass spectrometry in AGA (n = 20) and SGA infants (n = 20) and 91 DEPs were identified. Enrichment analysis revealed that they were related to complement and coagulation cascades, lipid metabolism, neural development, PI3K/Akt and RAS/RAF/MAPK signaling pathways, phagocytosis and focal adhesion. Protein-protein interaction (PPI) analysis identified 39 DEPs involved in the pathways enriched by the KEGG and Reactome. Those DEPs were associated with measures of adiposity and insulin resistance and with liver fat at age 7 (all < 0.01). Multivariate linear regression analysis uncovered that two DEPs (up-regulated in SGA), namely PCYOX1 (related to adipogenesis) and HSP90AA1 (related to lipid metabolism and metabolic-dysfunction-associated steatotic liver disease progression), were independent predictors of the hepatic fat fraction at age 7 (β = 0.634; = 0.002; R = 52% and β = 0.436; = 0.009; R = 24%, respectively). These data suggest that DEPs at birth may predict insulin resistance, adrenarche and/or ectopic adiposity in SGA children at age 7, when an early insulin-sensitizing intervention could be considered. - Source: PubMed
Publication date: 2025/02/18
Díaz MartaQuesada-López TaniaVillarroya FrancescCasano PaulaLópez-Bermejo Abelde Zegher FrancisIbáñez Lourdes