ATP6V1E1 Recombinant Protein
- Known as:
- ATP6V1E1 Recombinant Protein
- Catalog number:
- XW-RP3020
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ATP6V1E1 Recombinant Protein
Related genes to: ATP6V1E1 Recombinant Protein
- Gene:
- ATP6V1E1 NIH gene
- Name:
- ATPase H+ transporting V1 subunit E1
- Previous symbol:
- ATP6E, ATP6V1E
- Synonyms:
- P31, Vma4, ATP6E2
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-27
- Date modifiied:
- 2016-10-05
Related products to: ATP6V1E1 Recombinant Protein
Related articles to: ATP6V1E1 Recombinant Protein
- Intracellular pathogens such as Mycobacterium tuberculosis (Mtb) can promote their survival within infected cells by preventing lysosomal acidification. Here, we report that Mtb secretes a protein (Rv1184, or acyltransferase Chp2) that inhibits lysosomal acidification by targeting the host vacuolar ATPase (V-ATPase). We show that phosphorylation of the V-ATPase E1 subunit (ATP6V1E1) at Tyr56/57 suppresses lysosomal acidification through inhibition of V-ATPase assembly. Further investigation reveals that tyrosine kinase BMX promotes phosphorylation of ATP6V1E1. Strikingly, Chp2 increases BMX-dependent phosphorylation of ATP6V1E1, apparently by directly binding ATP6V1E1 and facilitating its interaction with BMX. Furthermore, inhibition of BMX impairs Mtb growth within macrophages and in mice. Thus, our work reveals a mechanism for the regulation of lysosomal acidification and suggests lysosomal acidification modulation as a potential approach for host-directed therapy against Mtb. - Source: PubMed
Publication date: 2026/02/06
Chen JianxiaTang FenQin LianhuaFang WeijunGuan LiruWu XiangyangLi HaohaoDuan YongjiaWang FeiPeng ChengLiu ZhonghuaWang JieHuang XiaochenWang LinYang HuaWang LiSha WeiCai XiaLyu Liang-DongLiu HaipengLiu FengGe BaoxueZheng Ruijuan - In avian species, the chorioallantoic membrane (CAM) is a vital, highly vascularized extraembryonic structure that supports embryonic respiration, calcium transport, and innate immune defense. In this study, we applied LC/MS/MS-based proteomics to CAM tissue harvested at embryonic days (ED) 6, 8, 10, and 12 to characterize its protein profile during the expression of different CAM functionalities during embryonic development and gain insight into possible sex-based distinctions. A total of 2688 proteins were identified, with 2347, 2265, 2351, and 1267 proteins detected at ED 6, 8, 10, and 12, respectively. Notably, 1191 common proteins were identified across all stages, while 124, 47, 86, and 2 proteins were uniquely expressed at ED 6, 8, 10, and 12, respectively. Functional annotation revealed correlations with abundant CAM protein constituents (as per their emPAI); for example: calcium mobilization - v-type proton ATPase subunit E1 (ATP6V1E1) and G1 (ATP6V1G1); intracellular transport-calcium-binding protein 39 (CAB39); vascular system and gaseous exchange - annexin A2 (ANXA2); lymphatics-actin, gamma 1 (ACTG1); blood elements-hemoglobin subunit alpha-1 (HBA1); immune defense-cathelicidin-1 (CATH1), cathelicidin-2 (CATH2); and protection against luminal toxic contents-thioredoxin (TXN). Notably, a sex-specific analysis identified 614, 320, 314, and 212 proteins that were uniquely expressed in female embryos, and 212, 273, 144, and 56 proteins only in male embryos at ED 6, 8, 10, and 12, respectively. The identification of sex-linked proteins during early CAM development may provide insight into their functional roles and highlight the CAM's potential as a target for the development of sex identification technology. - Source: PubMed
Publication date: 2025/12/24
Ali SofhianAhmed Tamer A EShrestha AgrimaHincke Maxwell T - The incidence of prostate cancer continues to increase, making it the second most common malignant tumor among men worldwide. Immunotherapy has emerged as a key therapeutic strategy for treating tumors. Numerous studies have established that the efficacy of tumor immunotherapy is closely associated with the tumor microenvironment and T cell subsets. However, the specific functions of certain T cell subsets in prostate cancer remain incompletely characterized. Therefore, this study aimed to systematically investigate the distribution patterns of T cell subsets within the tumor microenvironment of prostate cancer patients and their correlations with clinicopathological parameters. Therefore, we investigated the impact of T cells on the tumor microenvironment of prostate cancer at the single-cell level. We employed a variety of analytical methods to reveal the functions of T cells, including cell interaction analysis, time-series analysis, enrichment analysis, immune infiltration analysis, and other analytical approaches. By integrating bulk RNA-seq data, we constructed and validated a prognostic risk model based on T cell marker genes. Finally, we utilized the ssGSEA and ESTIMATE algorithms to explore the relationship between the prognostic risk model and immunotherapy. After quality control, 16,999 cells from the single-cell data were retained for downstream analysis. Our study focused on T cells, revealing the communication between various cell types and T cells. Pseudotime analysis showed that different T cell marker genes exhibited differential expression at various time points, corresponding to distinct biological processes. Enrichment analysis indicated that T cell marker genes were enriched in several immune-related pathways. From our analysis, BCAS2, EIF2S2, RIOK3, and ATP6V1E1 were ultimately identified as prognostic markers. Immune infiltration analysis revealed that high-risk patients had lower immune scores, stromal scores, and ESTIMATE scores and greater tumor purity compared to low-risk patients. We analyzed the mechanisms involving T cells in prostate cancer from multiple perspectives, constructed a prognostic model, and conducted immune infiltration analysis. Our findings contribute to the understanding of prostate cancer and its prognosis, providing valuable insights for future research and prognostic assessments in prostate cancer. - Source: PubMed
Publication date: 2025/12/31
Wang ZhiduXing YanShang DongmeiJin Xuefei - Alzheimer's disease (AD), a leading cause of dementia, is characterized by mitochondrial dysfunction, including impaired oxidative phosphorylation (OXPHOS), which drives neurodegeneration. This study aimed to identify OXPHOS-related AD biomarkers for early intervention. Integrated analysis of differentially expressed genes from AD temporal lobe and peripheral blood samples, using multivariate logistic regression and LASSO, identified ATP6V1E1 and NDUFB5 as key genes and potential AD risk factors. These genes exhibited strong diagnostic performance (AUC >0.7) and were validated in two independent cohorts. Further western blotting validation using an AD mouse model revealed that both genes were significantly downregulated in the hippocampus. Notably, their expression levels showed significant negative correlations with both Aβ and Tau pathology in AD mouse models. Single-cell RNA-seq analysis indicated their predominant expression in microglia, linking their expression to dysregulated immune cell infiltration. Furthermore, we observed a widespread downregulation of multiple mitochondrial complex I and V-ATPase subunits, indicating a systemic impairment in OXPHOS and lysosomal acidification in AD. This coordinated dysregulation underscores the synergistic dysfunction of mitochondrial and lysosomal systems in AD pathogenesis. This research highlights ATP6V1E1 and NDUFB5 as potential early AD indicators, and provides new insights into both the molecular mechanisms underlying AD pathogenesis and novel therapeutic strategies. - Source: PubMed
Publication date: 2025/11/14
Shao JunjieFan XiuzhaoTian ShuangshuangZhang FangLi JunhuZhao ZhiboLi YuanyuanZhou Xiaoshuang - SARS-CoV-2 non-structural protein 6 (NSP6) in the host's tissue-specific complexities remains a mystery and needs more in-depth attention because of COVID-19 recurrence and long COVID. Its reported role in immune evasion, viral replication and egress from the cells as well as its gain of function mutations occurring independently in various variants underscores its importance. - Source: PubMed
Publication date: 2025/10/22
Chatterjee ShrabontiMahata JoydeepKateriya SuneelAnirudhan Gireesh