PTGER3 _ EP3
- Known as:
- PTGER3 _ EP3
- Catalog number:
- Y214010
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PTGER3 _ EP3
Related genes to: PTGER3 _ EP3
- Gene:
- PTGER3 NIH gene
- Name:
- prostaglandin E receptor 3
- Previous symbol:
- -
- Synonyms:
- EP3
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2016-10-05
Related products to: PTGER3 _ EP3
Related articles to: PTGER3 _ EP3
- Stevens-Johnson syndrome (SJS) is a rare and severe mucocutaneous disorder often triggered by medications or infections. Our previous research identified that four key genes, Ikzf1, Ptger3, Mavs, and Tlr3 are involved in SJS susceptibility and the conjunctival epithelial innate immune response, demonstrating their role in regulating interferon-stimulated genes. However, the interplay among these regulatory factors remains unclear. This study aimed to elucidate the crosstalk mechanisms between the pathways regulated by these four genes in conjunctival epithelial cells. We constructed a comprehensive gene regulatory network using transcriptomic data from murine conjunctival epithelial cells under 16 distinct conditions, including polyI:C stimulation across wild-type, knockout, and transgenic backgrounds for the key genes. A targeted network analysis systematically identified numerous candidate genes mediating the crosstalk between the regulatory pathways initiated by Ikzf1, Ptger3, Mavs, and Tlr3. The identified candidates suggest the involvement of diverse signaling pathways previously unlinked to SJS pathology. Our findings suggest that the pathogenesis of SJS may arise not from the dysfunction of isolated genes but from the disruption of a balance maintained by intricate pathway crosstalk. - Source: PubMed
Publication date: 2026/06/18
Watanabe MakotoUeta MayumiNishigaki HiromiMizushima KatsuraNaito YujiKinoshita ShigeruSotozono ChieTakayama Jun - Metastasis is the primary cause of mortality in patients with breast cancer. This study aimed to develop a prognostic signature based on metastasis- and cancer-associated differentially expressed genes (M-CA-DEGs) and to identify potential novel therapeutic genes. - Source: PubMed
Publication date: 2026/05/11
Yao YuanZheng YunshengXie JiancongLiu HonghaoChen ChenCao JieYin Ting-Ting - Sanjie Xiaoliu Granule (SJXLG), a traditional multi-herbal prescription widely used in Chinese medicine, has been historically applied to "disperse nodules, soothe the liver, and relieve depression." It is clinically prescribed for patients with breast lumps, emotional stagnation, and cancer-related depression. However, the pharmacological basis underlying its dual anticancer and antidepressant effects remains poorly understood.This study aimed to evaluate the therapeutic efficacy and elucidate the molecular and metabolic mechanisms of SJXLG in breast cancer with depression (BCD) through integrated experimental and bioinformatics approaches. In vivo and in vitro BCD models were established to assess tumor growth, behavioral performance, and inflammatory cytokine levels. Liquid chromatography-mass spectrometry (LC-MS) identified active constituents of SJXLG. Bioinformatics analyses were used to screen key genes and signaling pathways, followed by validation via qRT-PCR and Western blot. Untargeted metabolomics was applied to explore the metabolic alterations in tumor tissues after SJXLG intervention. - Source: PubMed
Publication date: 2026/05/18
Liu ZhuoTong TianhaoYang RenyiZeng Puhua - Fried food and hazard factors, particularly acrylamide, have been implicated in adverse health outcomes. However, how fried food consumption fuels the development of metabolic associated fatty liver disease (MAFLD) remains poorly understood. - Source: PubMed
Publication date: 2026/04/26
Wan XuzhiLiu XiaohuiMeng DenghuiWang AnliSong XiaoranHuang YingyuZhang FanLin XunanYao JianxinZheng YouyouLu QiTian YimeiFan YileiZhuang PanJiao JingjingZhang Yu - BACKGROUND: Colorectal cancer (CRC) remains a significant cause of global cancer mortality. While aspirin demonstrates therapeutic benefits, the molecular determinants underlying patient response are poorly understood, hindering personalised treatment strategies. This study aimed to identify molecular subtypes in CRC based on prostaglandin pathway markers and assess their association with clinical outcomes and aspirin use. METHODS: We analysed paired tumour and adjacent normal tissues from 86 CRC patients (43 regular aspirin users, 43 aspirin-free) via qPCR for mRNA expression (PTGS1, PTGS2, PTGER2, PTGER3) and immunohistochemistry for protein levels (COX-2, Caspase-8, MMP-9). Normalised expression data were correlated with clinicopathological features and survival. Unsupervised clustering algorithms (K-means, hierarchical, and hybrid) were applied independently to each cohort to identify distinct molecular subtypes using Z-score-normalised data across all seven markers. RESULTS: Aspirin-treated patients showed significantly higher PTGS2 and PTGER3 mRNA, elevated Caspase-8 protein, and reduced MMP-9 protein compared to the aspirin-free group. Unsupervised clustering identified distinct molecular subtypes within both cohorts. In the Aspirin-Treated group, clinical stratification yielded a two-subtype solution (AT-1, AT-2), primarily driven by differential protein expression (Caspase-8, COX-2, MMP-9), which demonstrated a trend towards distinct survival outcomes (P = 0.073). In the Aspirin-Free group, a clinically relevant two-subtype solution (AF-1, AF-2) demonstrated significant survival differences (47.4% vs 16.7%, P = 0.016); the poor-prognosis subtype (AF-2) was characterised by higher PTGS2 mRNA, higher COX-2 protein, lower Caspase-8, and higher MMP-9 levels. Notably, strong correlations between PTGS2 mRNA and adverse clinical outcomes observed in the aspirin-free cohort were absent in the aspirin-treated group. CONCLUSION: Integrated prostaglandin pathway gene and protein expression analysis identifies distinct CRC molecular subtypes with prognostic significance, particularly related to aspirin use. Key protein markers (Caspase-8, COX-2, MMP-9) and PTGS2 mRNA levels differentiate these subtypes. Aspirin treatment disrupts specific molecular correlations linked to prognosis, suggesting modulation of post-transcriptional networks. These findings support the use of multi-marker molecular profiles to improve patient stratification and personalised aspirin therapy in CRC. - Source: PubMed
Publication date: 2026/04/14
Mostafavi-Fini Hanieh-SadatMoradi ArashGowdini ErfanMohammadi RamtinAbdollahi TinaJamshidian FaranakGanji Shahla Mohammad