Ask about this productRelated genes to: ENPP2 Blocking Peptide
- Gene:
- ENPP2 NIH gene
- Name:
- ectonucleotide pyrophosphatase/phosphodiesterase 2
- Previous symbol:
- PDNP2
- Synonyms:
- ATX, PD-IALPHA
- Chromosome:
- 8q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-10
- Date modifiied:
- 2015-09-11
Related products to: ENPP2 Blocking Peptide
Related articles to: ENPP2 Blocking Peptide
- Choline is an essential nutrient required for the synthesis of key molecules, such as phosphatidylcholine, sphingomyelin, acetylcholine, and S-adenosylmethionine. Choline metabolism encompasses two phases, namely the postprandial and postabsorptive states. The former enables the digestion, absorption, distribution, and storage of choline derivatives after a meal, while the latter allows the cellular utilization of choline and the mobilization of stored choline-containing molecules during fasting. Understanding choline metabolism is fundamental to the study of lipid disorders such as steatohepatitis or atherosclerosis, as well as neurodegenerative diseases, including Alzheimer's disease, and inflammatory signaling pathways. Members of the alkaline phosphatase (AP) superfamily are prominent contributors to extracellular choline metabolism. Within this family, several APs and ectonucleotide pyrophosphatases/phosphodiesterases (ENPP) members are required for physiological choline metabolism. While intestinal alkaline phosphatase (IAP) and alkaline sphingomyelinase/ENPP7 both participate in the digestion of choline-containing derivatives in the gut during the postprandial phase, circulating ENPP2, ENPP6, and tissue-nonspecific alkaline phosphatase (TNAP) act during the postabsorptive phase to generate choline. In this review we first provide a comprehensive overview of choline metabolism and then describe how APs and ENPPs have functionally and structurally co-evolved to catalyze sequential reactions within this metabolic pathway. - Source: PubMed
Publication date: 2026/04/30
Lecornu FélixDrevet Mulard EvaBessueille LaurenceGerardin DaliaRautureau Gilles Jean PhilippeBallut LionelMagne David - Liver cirrhosis(LC) represents the end stage of chronic liver disease, yet reliable molecular markers remain limited. This study aimed to uncover potential diagnostic biomarkers and therapeutic targets for LC. - Source: PubMed
Publication date: 2026/03/14
Zhang KangChen TingJia ZhangyuZhao JunxiaHuang Na - Immune checkpoint inhibitors (ICI), including those that block PD-1/PD-L1, have revolutionized therapy for patients with non-small cell lung cancer. However, most patients demonstrate no clinical benefit or acquire resistance, even when tumors express PD-L1. This highlights the critical need to dissect tumor survival dependencies to overcome resistance. Using our Kras/p53-driven lung cancer models that demonstrate acquired or intrinsic resistance to ICI, we performed single-cell RNA sequencing and focused on predicted upstream regulators of differentially expressed genes in the malignant cell cluster of resistant tumors. We found that the micro-RNA miR-29 was downregulated in tumors with anti-PD-1 resistance, and that this was associated with significant upregulation of a multitude of miR-29 targets. Furthermore, we found expression of Enpp2/ATX, a gene encoding an immunosuppressive molecule, was modulated due to miR-29 loss. Re-expression of miR-29 in anti-PD-1 resistant models reduced ATX expression in tumor cells, diminished the fibrotic microenvironment, and increased CD8+ T-cell infiltration. These alterations promoted response to ICI in an anti-PD-1 resistant model by rewiring the tumor immune microenvironment, specifically through increased CD8+ T-cell infiltration, reduction of suppressive Ly6C+ monocytes, and a concomitant increase in pro-inflammatory macrophages. Additional analysis of publicly available RNA-sequencing data revealed tumors from lung adenocarcinoma patients with high miR-29 had increased CD8A and decreased CD14 expression, and broad enrichment in immunoregulatory pathways. Together, these data provide evidence that the miR-29 family regulates the tumor microenvironment, including antitumor immune-related pathways in lung cancer, through control of ATX among other target genes, with implications for ICI response. - Source: PubMed
Publication date: 2026/02/25
Horvat Natalie KSaint-Cloud MyritneyBint Abdullah Muslim RaihaanahTian YanhuaRodriguez B LeticiaHall Margaret ALabani-Motlagh AlirezaDiao LixiaWang JingLesinski Gregory BMoffitt Richard AGibbons Don LKonen Jessica M - We investigated whether basement membrane (BM) laminins influence regional differences in the vasculature by performing single-cell RNA sequencing on cerebral blood vessels from mice lacking the major vascular laminins in endothelial and smooth muscle BMs, laminin α4 ( ) and laminin α5 (), and wild-type littermates. Our dataset expands existing cerebral vascular transcriptomic profiles and reveals that endothelial cells exhibit increased arterial marker expression and reduced postcapillary venule identity. In vitro and in vivo studies indicated that compensatory upregulation of laminin α5 in vessels enhances expression of junctional proteins (, ) and promotes vessel contractility via increased expression of contractile molecules in mural cells. Additionally, loss of upregulated expression of large artery markers (, , ) and resulted in elevated autotaxin () levels, a key enzyme in lysophosphatidic acid production implicated in stroke. Accordingly, mice exhibited worsened stroke outcomes, driven not by immune infiltration or junctional defects, but by increased vascular permeability likely mediated by autotaxin and/or activation of resident myeloid cells. Our data suggest that laminin α4/α5 ratios in vascular BMs affect functional zonation between arterioles, capillaries and postcapillary venules by modulating metabolic pathways in endothelial and mural cells, and indirectly influencing resident myeloid cells. - Source: PubMed
Publication date: 2026/02/16
Deshpande TusharKapupara KishanHannocks Melanie-JaneHuppert JulaSamawar Sai-KiranThulichery Devika RagBudny SigmundGhavampour SharangSong JianMeng LingzhangAdams Ralf HJeong Hyun-WooWachsmuth LydiaFaber CorneliusSoltwisch JensHallmann RupertSorokin Lydia - Hypertrophic cardiomyopathy (HCM) is a condition where approximately 65% of patients exhibit myocardial fibrosis, indicated by late gadolinium enhancement, with the severity and extent of fibrosis being positively correlated with the risk of sudden cardiac death. While fibroblast activation in HCM has been noted in previous studies, the underlying regulatory mechanisms have not been thoroughly explored. In this study, we analyzed the latest single-nucleus sequencing (snRNA-seq) datasets related to HCM caused by the two most common mutations. We also examined the largest existing snRNA-seq and spatial transcriptomics datasets of HCM for external validation. Additionally, we conducted preliminary histopathological and molecular biology experiments to validate our findings and explore potential mechanisms. Our analysis revealed a phenotypic transformation of macrophages in both cases of HCM. These pro-inflammatory macrophages, driven by the high expression of ENPP2, mediated intercellular interactions that influenced fibroblast activation. The resulting increase in lysophosphatidic acid appeared to act as a plausible intermediary. Activated fibroblasts secreted substantial amounts of COL14A1, which is a critical component of myocardial fibrosis. These findings were consistent across different genetic backgrounds, suggesting their universal applicability in most HCM cases. Our study provides valuable insights into the mechanisms underlying myocardial fibrosis in HCM, highlighting the role of macrophage transformation and fibroblast activation. These findings offer potential for the identification of novel diagnostic or prognostic biomarkers and the development of targeted therapies with clinical translational potential. - Source: PubMed
Huang FanyiZhou MiChen YanjiaHua ShaHan YanxinFan YingzeLi QingchuanSun ZhuoyanYang KeZhao QiangJin Wei