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
- Acquired drug resistance is a major cause of failure in gastric cancer treatment. The protein tyrosine phosphatase receptor type E (PTPRE) plays an oncogenic role in certain tumours; however, its function in chemotherapy-resistant gastric cancer remains unclear. Therefore, we analysed PTPRE expression in gastric cancer using The Cancer Genome Atlas. In vitro experiments were then conducted to investigate the effects of PTPRE on the resistance of cancer cells to 5-fluorouracil (5-FU) and its potential mechanisms. The results were further validated in vitro using xenograft studies. We found that PTPRE is upregulated in gastric cancer tissues and participates in the induction of 5-FU resistance. Mechanistic studies revealed that PTPRE suppressed ferroptosis in gastric cancer cells and promoted 5-FU resistance by activating the Src/FAK pathway to upregulate TRIB3 expression. In summary, PTPRE suppresses ferroptosis in gastric cancer cells via the Src/FAK/TRIB3 signalling pathway, thereby inducing 5-FU resistance. Intervention with PTPRE and its downstream targets may represent a potential approach for the clinical treatment of 5-FU-resistant gastric cancer. - Source: PubMed
Publication date: 2026/06/18
Liu MingLiao XiaomeiWang FangchaoJiao PengqingWang Zhongkai - 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