Ask about this productRelated genes to: PTPRE antibody
- Gene:
- PTPRE NIH gene
- Name:
- protein tyrosine phosphatase receptor type E
- Previous symbol:
- -
- Synonyms:
- PTPE
- Chromosome:
- 10q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-12
- Date modifiied:
- 2019-02-14
Related products to: PTPRE antibody
Related articles to: PTPRE antibody
- Prior studies have identified atypical expression of protein tyrosine phosphatase receptor type E (PTPRE) in animal models of salt-sensitive hypertension (SSH). This study investigates PTPRE's role in SSH and clarifies its mechanism of action. Through gene knockdown and overexpression of PTPRE in DOCA-salt hypertensive mice, we assessed the vasomotor function of aortic rings. PTPRE-induced phenotypic changes in vascular smooth muscle cells (VSMCs) were identified using phenotypic markers and related functional parameters. The phosphorylation levels of the MAPK signaling pathway subfamilies were assessed using Western blot analysis. Upregulation of PTPRE was observed in the VSMCs of DOCA-salt-induced SSH mice. This upregulation was associated with impaired vasoconstriction and vasodilation of arteries, as well as increased blood pressure (BP) (all p < 0.01). Altering PTPRE expression via knockdown and overexpression markedly affected the expression of synthetic (OPN) and contractile (α-SMA and SM22α) phenotype markers in the aortic media and VSMCs of SSH mice (all p < 0.01). Moreover, PTPRE expression influenced the phosphorylation activation within the MAPK signaling pathway. Specifically, regulation of PTPRE expression in SSH modulated the phosphorylation of the JNK and p38 MAPK subfamilies, along with the upstream phosphorylation of MKK3 and MKK6 (all p < 0.05). Our findings indicate that PTPRE significantly contributes to vascular vasomotor dysfunction and the phenotypic transformation of VSMCs in SSH. This involvement in SSH development seems to occur mainly via modulation of the JNK and p38 MAPK pathways. - Source: PubMed
Li Shi-ChengWang HaoShao Qiao-YuZhang Jia-HaoZeng Meng-YingBian Wei-KangWang Fang-LuFeng Shu-YiYan Xiao-WeiZhang Shu-Yang - The mechanisms underlying tumor evolution and treatment resistance in locally advanced head and neck squamous cell carcinoma (LA-HNSCC) are not fully understood. This study used whole-exome sequencing (WES) of paired tumor tissue and circulating tumor DNA (ctDNA) to analyze intratumoral heterogeneity (ITH) and clonal dynamics at diagnosis and relapse. - Source: PubMed
Publication date: 2025/11/20
Bruixola GMartín-Arana JGimeno-Valiente FCarbonell-Asins J AGarcía-Micó BMartínez-Castedo BGonzález-Camblor DGrimalt NGarcía-Bartolomé MAlfaro-Cervelló CEscorihuela VIglesias M EMaroñas MDualde DCervantes ATarazona N - Bats are recognized for harboring a diverse array of viruses without manifesting disease symptoms. In this study, we explored the single-cell atlas of wild Rhinolophus affinis (R. affinis) using Viral-Track and identified transcript expression of eight viral species in the R. affinis lung and three viral species in the kidney. Within the R. affinis lung, these viruses were detected across all cell types except ciliated cells. Compared to uninfected cells, virus-infected cells exhibited activation of pathways associated with protein synthesis, tissue repair, and immune responses, as evidenced by increased expression of corresponding genes. Ligand-receptor based analysis revealed that viral infection reshapes intercellular communication networks in the bat lung, with infected fibroblasts and infected proliferative T cells exhibiting enhanced signaling linked to tissue remodeling and immune activation. Through gene module analysis, we identified an immune cell activation-related module by high expression of CD14, CD74, and MRC1, as well as an antiviral related module by elevated expression of SAMHD1, SLC11A1, TYROBP, and IL18 in R. affinis pulmonary macrophages. Additionally, a cross-species single-cell transcriptomic comparative analysis demonstrated that R. affinis pulmonary macrophages exhibit elevated expression of pro-inflammatory genes (IRF9, DDX5, IL6ST and ITGA4), which are associated with antiviral activity and immune activation, and anti-inflammatory genes (IRF2, PTPRE and GPR65), which play critical roles in mitigating excessive immune responses. Compared to the other species, R. affinis pulmonary macrophages exhibited upregulation of genes enriched in pathways related to vacuolar acidification and negative regulation of response to external stimulus. These findings suggest that the R. affinis lung possesses a unique immune system that enables it to balance immune responses during viral infections, thereby preventing excessive immune damage and maintaining lung tissue homeostasis. Our study provides valuable insights into the viral infection risk organs in R. affinis and their distinctive antiviral immune responses. - Source: PubMed
Publication date: 2025/11/07
Lv TianhangZhang JianhuiZheng ZhiwanFan Xiaohui - The molecular pathophysiology underlying the development of bronchiectasis with exacerbation at the proteomic level has not been clarified using bronchoalveolar lavage fluid samples. This study aimed to evaluate the bronchoalveolar lavage fluid inflammatory profiles associated with exacerbation of bronchiectasis. - Source: PubMed
Publication date: 2025/10/01
Lee Ju YeonYang JiyoulKim Jin YoungDo YejiKim Min-SikKye Dong EunMin GeonhuiJeon In-SookKim Eung-GookChoi Joong KookChoi MinjaeLee HyunYang Bumhee - Existing genetic studies of neuroticism have been largely limited to common variants. Here we performed a large-scale exome analysis of white British individuals from UK Biobank, revealing the role of coding variants in neuroticism. For rare variants, collapsing analysis uncovered 14 neuroticism-associated genes. Among these, 12 (PTPRE, BCL10, TRIM32, ANKRD12, ADGRB2, MON2, HIF1A, ITGB2, STK39, CAPNS2, OGFOD1 and KDM4B) were novel, and the remaining (MADD and TRPC4AP) showed convergent evidence with common variants. Heritability of rare coding variants was estimated to be up to 7.3% for neuroticism. For common variants, we identified 78 significant associations, implicating 6 unreported genes. We subsequently replicated these variants using meta-analysis across other four ancestries from UK Biobank and summary data from 23andMe sample. Furthermore, these variants had widespread impacts on neuropsychiatric disorders, cognitive abilities and brain structure. Our findings deepen the understanding of neuroticism's genetic architecture and provide potential targets for future mechanistic research. - Source: PubMed
Publication date: 2024/11/07
Wu Xin-RuiLi Ze-YuYang LiuLiu YingFei Chen-JieDeng Yue-TingLiu Wei-ShiWu Bang-ShengDong QiangFeng Jian-FengCheng WeiYu Jin-Tai