ENPP2_RAT Enpp2 ELISA tesk kit
- Known as:
- ENPP2_RAT Enpp2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15789
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ENPP2_RAT Enpp2 ELISA tesk kit
Related genes to: ENPP2_RAT Enpp2 ELISA tesk kit
- 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_RAT Enpp2 ELISA tesk kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Sizeα - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit Related articles to: ENPP2_RAT Enpp2 ELISA tesk kit
- Chronic exposure to ultraviolet B (UVB) radiation induces excessive reactive oxygen species (ROS) production in dermal fibroblasts, leading to cellular senescence and skin photoaging. Ageing skin is characterised by disruption of the immune microenvironment, including impaired macrophage polarisation and reduced M2 macrophage activity. However, the contribution of M2 macrophages to fibroblast photoaging remains incompletely understood. Here, we investigated whether M2 macrophages attenuate UVB-induced fibroblast senescence through ectonucleotide pyrophosphatase/phosphodiesterase 2 (ENPP2)-dependent lysophosphatidic acid (LPA)signalling. UVB-induced L929 fibroblasts were treated with conditioned media derived from polarised RAW264.7 macrophages, with or without ENPP2 silencing. UVB exposure induced marked senescence, oxidative stress, and mitophagy impairment, whereas conditioned medium from M2 macrophages significantly alleviated these effects compared with M1-derived conditioned medium. Notably, ENPP2 depletion in M2 macrophages substantially reduced these protective effects. M2 macrophage-derived conditioned medium contained elevated LPA levels and restored UVB-suppressed LPAR1 and LPAR3 expression in fibroblasts. Pharmacological inhibition of LPAR1/3 attenuated the protective effects of M2 macrophages, while exogenous LPA supplementation restored these effects under ENPP2-deficient conditions. These changes were associated with enhanced PINK1/Parkin-related mitophagy signalling and reduced oxidative stress. Collectively, these findings identify M2 macrophage-derived ENPP2/LPA signalling as a critical paracrine mechanism that mitigates UVB-induced fibroblast photoaging. - Source: PubMed
Lu MeiqiWang XiaoyangHu YujieJia ShanshanQi YongjunJiao YaZhao JieWang XiaochuanZhang JixunJiang Duyin - Therapeutic resistance limits durable survival in advanced/metastatic renal cell carcinoma (RCC) treated with first-line tyrosine kinase inhibitor (TKI) plus immune checkpoint inhibitor (ICI). We sought to define key resistance drivers and actionable targets. - Source: PubMed
Publication date: 2026/06/29
Luo JinchenLin HansenFeng HaoqianTan LeiLiu XiHuang YongCen JunjieChen JiajieZhou XinweiLin MingjieLiao WuyuanAi ZheyuChen MinyuWang YinghanChen WeiLuo JunhangLiang Yanping - Pancreatic cancer remains one of the most lethal malignancies, characterised by aggressive progression, metabolic adaptation, and resistance to therapy. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical mechanism influencing tumour survival and therapeutic response. However, the role of ferroptosis suppressor genes (FSGs) in pancreatic cancer remains incompletely understood. In this study, FSGs were systematically retrieved from FerrDb V2 and subjected to multi-step filtering to identify a curated set of 196 protein-coding genes. Genomic alteration analysis using cBioPortal across 21 pancreatic cancer studies (n = 5189 samples) identified seven recurrently altered genes (TP53, HSF1, PARP10, ZFP36, SIRT2, ECH1, and ENPP2) with alteration frequencies ≥ 3%. Co-occurrence analysis revealed predominantly cooperative alteration patterns among these genes, suggesting functional complementarity. Survival analysis demonstrated that alterations in FSGs were significantly associated with reduced overall survival in pancreatic cancer, with several genes (ECH1, ZFP36, SIRT2, and ENPP2) showing particularly strong adverse prognostic effects. In contrast, no significant survival associations were observed in oesophageal and gastric cancers, indicating a tumour-specific dependency on ferroptosis-related mechanisms. KEGG pathway enrichment analysis of the broader FSG set revealed significant involvement in pathways related to metabolic regulation (AMPK-mTOR signalling), autophagy, hypoxia response (HIF-1 signalling), and oncogenic signalling (PI3K-Akt pathway). Integration of these findings suggests that ferroptosis suppressor genes contribute to pancreatic cancer progression by promoting metabolic adaptation and resistance to oxidative stress. In conclusion, this study identifies key ferroptosis suppressor genes with prognostic relevance in pancreatic cancer and highlights their integration within critical metabolic and stress-response pathways. The tumour-specific nature of these associations underscores the importance of biological context and supports the potential of FSGs as prognostic biomarkers and potential therapeutic targets in ferroptosis-based strategies. - Source: PubMed
Publication date: 2026/06/10
Singh Nitin KumarSingh ManinderHusain AdilAlnajjar Lina IAhmad FirozMishra Siddhartha KumarAlshamamri NawafSaeed MohdRab Safia ObaidurGupta Varsha - Phenolic endocrine-disrupting chemicals (EDCs) like nonylphenol (NP) and octylphenol (OP) are widespread water pollutants. Their estrogen-like properties are suspected contributors to prostate cancer, but their precise molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/06/02
Zhu XinyaoWu QilongLi YuqiLiu ZhiyuZeng YangZeng ZhiqiangZhou YuboZou LunhongWu XiaochunZhao DanDeng QingfuZhou Tao - ENPP1 is emerging as a potential target for cancer immunotherapy due to its negatively regulatory effect on the STING pathway via hydrolysis of cGAMP. Herein, we report the identification and optimization of compound starting from hit compound . is a potent and selective ENPP1 inhibitor featuring a novel pyrrolo[1',2':1,6]pyrimido[5,4-]pyridazin-6(5)-one core scaffold. It exhibited substantial inhibitory activity against ENPP1 with an IC value of 9.5 nM, while showing weak inhibition against ENPP2/3. In the cGAMP-mediated STING pathway, this compound effectively enhanced the expression of downstream genes and promoted the phosphorylation of the relevant protein. Moreover, it displayed favorable pharmacokinetic properties and no evident cytotoxicity. In a 4T1 syngeneic mouse model, oral administration of compound demonstrated significant antitumor effects and enhanced the efficacy of both anti-PD-1 antibody and chemotherapy, with good tolerability. Collectively, these results highlight the potential of compound to potentiate STING-mediated antitumor immunity. - Source: PubMed
Publication date: 2026/05/26
Nong CuijieZhu MengyuanZheng WeilunYang JiachengWang HaidiLi ChuanghuiWen BojieLiu YuZhu XiaoyuZhu TaoXu YuHui HuiLai Yisheng