ATP6V1A Antibody
- Known as:
- ATP6V1A Antibody
- Catalog number:
- XW-8167
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ATP6V1A Antibody
Related genes to: ATP6V1A Antibody
- Gene:
- ATP6V1A NIH gene
- Name:
- ATPase H+ transporting V1 subunit A
- Previous symbol:
- VPP2, ATP6A1, ATP6V1A1
- Synonyms:
- Vma1, VA68
- Chromosome:
- 3q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-03
- Date modifiied:
- 2016-02-11
Related products to: ATP6V1A Antibody
Related articles to: ATP6V1A Antibody
- Environmental lead (Pb) exposure and high-fat diet (HFD) intake are known to trigger massive neuronal apoptosis that contributes to neurologic dysfunction. Previous studies mainly focused on isolated mitochondrial dysfunction, autophagy-lysosomal pathway damage, and neuronal apoptosis from Pb or HFD. Nevertheless, the precise role of the lysosomal and proteasomal clearance processes in promoting neuronal cell death induced by Pb and HFD remains unclear. In this study, male Sprague-Dawley (SD) rats were employed to elucidate the mechanisms underlying Pb-induced neurotoxic mitochondrial apoptosis and to investigate the effects of co-exposure to HFD. In vitro, PC12 cells were treated with Pb and palmitic acid (PA) to mimic the in vivo conditions. Specifically, such exposures prompted the translocation of cathepsin B (CTSB) from lysosomes to the cytosol and downregulation of lysosomal-associated membrane protein 1 (LAMP1), ATPase H⁺ Transporting V1 Subunit A (ATP6V1A), and Bcl-2 within rat cortex. In contrast, the levels of pro-apoptotic factors including BID, Bax, mitochondrial cytochrome C (Cyt C), and caspase 3 were significantly elevated. We also observed a significant decrease in the fluorescence intensity of lysosomes while lysosomal pH was ascertained to have ascended appreciably. Concurrently, CTSB inhibition by CA-074 me prevented neural apoptosis processing triggered by Pb and/or PA via mitigating lysosomal damage and mitochondrial Cyt C translocation, indicating that CTSB is a key mediator in the apoptotic process induced by Pb and HFD. - Source: PubMed
Publication date: 2026/04/28
Yuan YongkeLiu MengchenZhai MengdiWu MeijiaZhang WenhuiXin YongjuanBa YueZhang YuHan LinGao LihuaHuang Hui - Mitochondrial protein import and transporter systems play essential roles in maintaining metabolic competence and proteostasis in stem cells. However, the transcriptional architecture of mitochondrial translocase (TOM/TIM) complexes and transporter genes in human spermatogonial stem cells (SSCs) remains poorly defined. We performed an integrative analysis combining bulk microarray profiling of human SSC-enriched populations (n=3 biological replicates per group) with complementary single-cell RNA-sequencing (scRNA-seq) datasets. Differential expression (limma; |log₂FC| ≥ 2, adj. P < 0.05), co-expression network construction (WGCNA), protein-protein interaction mapping (STRING/cytoHubba), and miRNA-mRNA regulatory inference were used to identify key mitochondrial transporter nodes. Validation of hub-gene expression patterns was performed using an independent scRNA-seq dataset. Cell-type identity of SSC-enriched cultures was confirmed by immunocytochemistry for established SSC markers. Integrated multi-omics analyses revealed a coordinated enrichment of mitochondrial transporter genes in SSCs, including upregulation of TOMM and TIMM family members and selected ATPase and SLC transporters relative to fibroblasts. Hub genes (TOMM22, TIMM17A, ATP6V1A, SLC25A3) showed high network centrality and were consistently enriched in undifferentiated SSC clusters across multiple scRNA-seq datasets. miRNA-mRNA interaction modeling identified several SSC-expressed miRNAs (e.g., hsa-miR-4732-3p, hsa-miR-6503-3p) as potential post-transcriptional regulators of mitochondrial transporter networks. Human SSCs exhibit a distinctive mitochondrial transporter gene program characterized by enhanced expression of protein-import machinery and metabolic transport components. These findings provide a comprehensive molecular framework for understanding mitochondrial regulation in SSCs and establish new candidate targets for probing germline metabolism and stem-cell maintenance. - Source: PubMed
Publication date: 2026/03/02
Mahforoozmahalleh Zahra HasaniAzizi HosseinSkutella Thomas - Conventional drug screening platforms struggle to recapitulate native subcellular microenvironments, leading to high off-target rates and compromised discovery of bioactive compounds. To address this, we developed subcellular target-tracking fluorescent-visualization-based interaction screening (SubTrack-FVIS), a platform combining super-resolution imaging with target-specific fluorescent tagging. SubTrack-FVIS first maps nanoscale spatial distributions of drug targets within living cells, then screens compound libraries to identify molecules specifically binding to target-enriched domains, and finally quantifies drug-target interactions through super-resolution imaging tracking. Compared to traditional toolbox, SubTrack-FVIS reduces off-target effects by evaluating compound binding within native subcellular architectures. When applied to the lysosomal vacuolar H-ATPases (V-ATPase) subunit, ATP6V1A, a validated anti-cancer target, this approach identified for lysosomal alkalization fluorescent drug (LAFD) as a potent inhibitor. Super-resolution imaging revealed LAFD's dynamic binding to ATP6V1A clusters, enabling real-time visualization of V-ATPase inhibition and subsequent lysosomal destabilization. Crucially, SubTrack-FVIS uncovered LAFD's unique mechanism of blocking autophagosome-lysosome fusion, resolving autophagic flux obstruction at sub-100 nm resolution. This platform establishes a visualization framework for discovering drugs within physiological subcellular contexts while simultaneously decoding their mechanistic impacts, offering application potential for target-centric drug development. - Source: PubMed
Publication date: 2025/07/31
Wang RanYuan YatongShao HuarongSun YuehaoLai ChangchengZhang MengruiSong WenjingZhang TaoZhuang FengfengChen QixinLing PeixueShao Xintian - Blood and meat spots (BMS) are common internal defects in chicken eggs that compromise egg quality. To reveal genes contribute to BMS formation, we performed an Adaptive Lasso-based genome-wide association study (ALGWAS) of Rhode Island Red (RIR) hens. The results showed that the heritability of BMS was 0.13. Based on ALGWAS, we identified one significant and 144 suggestive SNPs associated with BMS. Within the significant locus, eight candidate genes were annotated (TNFRSF1A, CECR1, TRIM45, CALD1, SIDT1, VTCN1, USF3, ATP6V1A). Among these, VTCN1 emerged as the strongest candidate, supported by eQTL annotation and its established function as an immune checkpoint regulator that modulates inflammation, vascular integrity, and T-cell responses. - Source: PubMed
Publication date: 2026/02/17
Ma XiaolongChen XingCheng XueLiu WeiNing Zhonghua - In this exploratory pilot study, we profiled human periodontal ligament (PDL) transcriptomes during early orthodontic tooth movement (OTM). Early-stage (0-10 days) transcriptional dynamics under tension and compression remain insufficiently understood, and no dedicated user-friendly resource has been available for exploring large-scale human data. - Source: PubMed
Publication date: 2026/02/18
Zhang XiaoqiXing LuAi-Gumaei WaseemZhang XiaoqianWang QingxuanLi MinqiLong HuLai Wenli