ATP6V0C
- Known as:
- ATP6V0C
- Catalog number:
- 002250A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP6V0C
Related genes to: ATP6V0C
- Gene:
- ATP6V0C NIH gene
- Name:
- ATPase H+ transporting V0 subunit c
- Previous symbol:
- ATPL, ATP6C, ATP6L
- Synonyms:
- VATL, Vma3
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-12
- Date modifiied:
- 2016-02-11
Related products to: ATP6V0C
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- Neurodegenerative disorders are clinically and genetically heterogeneous, characterized by progressive neuronal loss and multidomain functional decline. Despite a presumed genetic etiology, a substantial proportion of cases remain molecularly undiagnosed. - Source: PubMed
Publication date: 2026/09/14
Zheng Ze-HongYuan Ru-YingFang Min-KunLin Hua-SongXiao Wen-HaoQiu Yu-SenCheng BiLin WeiGan Shi-RuiWang NingZeng Yi-HengChen Wan-Jin - Patients with sepsis exhibit circadian disruption and persistent immunosuppression. However, the molecular mechanisms linking them remain unclear. Integration of multi-cohort transcriptomic and single-cell datasets shows that circadian gene dysregulation in patients with sepsis and septic mice correlates with disease severity and immunosuppressive states, with monocytes/macrophages emerging as a principal affected population. Sustained endotoxin stimulation elevates the core clock repressor NR1D1 in macrophages, which occupies the Igf2bp2 promoter and suppresses its transcription. Loss of IGF2BP2 destabilizes the V-ATPase subunit transcripts Atp6v1b2 and Atp6v0c through an mA-dependent mechanism, disrupting phagolysosomal acidification rhythms and pathogen clearance. siRNA-mediated NR1D1 knockdown restores IGF2BP2 expression, circadian oscillations, and phagolysosomal function during the development of endotoxin tolerance. To achieve therapeutic delivery, we engineer hybrid membrane nanovesicles (siNR1D1@HM-LNP) that reverse circadian and immune dysregulation in septic mice, enhance bacterial clearance, and markedly improve survival. These findings establish an NR1D1-mediated circadian-immune coupling mechanism and provide a therapeutic strategy for targeting sepsis-induced immunosuppression. - Source: PubMed
Publication date: 2026/08/24
Chen LangLin WenyiJiang LangGao XuehuiYu ChenyanHan JiliLiu ZhenpingLi XuefengHe MeiLi ChangLi QilanSong ChaoyingXu JiqianShang You - Fever can trigger seizures in several early-onset epilepsies. SCN1A-related epilepsies, including Dravet Syndrome, are the best characterised conditions in this spectrum, but a growing number of genes implicated in fever-sensitive epilepsies have emerged. We assessed the genetic heterogeneity of individuals who underwent testing because of seizures or epilepsy with fever sensitivity. In particular, we investigated the occurrence of ATP6V0C pathogenic variants and delineated its associated electro clinical features. - Source: PubMed
Publication date: 2026/07/25
Tanganelli Federica Martina AbigailDi Feo Maria FrancescaMadia FrancescaChiarella LorenzoPiccinni AlbertoCanale EdoardoAmadori ElisabettaNobile GiuliaPrato GiuliaVari StellaGiacomazzi VeraStriano PasqualeNobili LinoZara FedericoFaravelli FrancescaMancardi Maria Margherita - Emerging evidence suggests that microglia exhibit dual regulatory roles in the pathogenesis of Parkinson's disease (PD); however, their precise function in α-synuclein clearance remains incompletely understood. Here, we provide compelling evidence that α-synuclein preformed fibrils (α-syn PFF) impair lysosomal acidification in microglia, leading to defective autophagic flux and disrupted α-syn degradation. This dysfunction further promotes the secretion of microglial extracellular vesicles (EVs), exacerbating disease pathology. Mechanistic investigations uncover that α-syn PFF directly interacts with ATP6V0C, a pivotal V0 subunit of V-ATPase. This interaction sterically hinders V0-V1 domain assembly, disrupting proton pump complex formation and reducing ATP6V0C expression. Functionally, ATP6V0C overexpression rescues lysosomal acidification deficits and facilitates α-syn degradation in vitro, while in vivo, ATP6V0C overexpression alleviates neurotoxicity and reduces phosphorylated α-syn aggregation in α-syn PFF mouse models. Further investigation identifies the PI3K-AKT-mTOR-TFEB pathway as a key regulatory axis of ATP6V0C-mediated lysosomal acidification in microglia. Notably, both TFEB activation and mTOR inhibition restore lysosomal acidity and upregulate ATP6V0C expression, thereby enhancing α-syn clearance. These findings establish the TFEB-ATP6V0C axis as a key determinant of microglial proteostasis, proposing targeted activation of this pathway as a promising strategy to mitigate PD progression. - Source: PubMed
Publication date: 2026/06/30
Wang YimingMa ZhuoranJin ZongjieKou LiangXiong NianWang TaoXia Yun - Granular cell dermatofibroma (GCDF) is a unique histopathological variant of dermatofibroma, characterized by a portion of the lesion composed of cells with abundant granular cytoplasm, resembling granular cell tumors (GCT). GCTs are associated with mutations in V-ATPase component genes; however, the pathogenesis and molecular alterations in GCDF remain uncharacterized. We performed whole exome sequencing on six GCDF cases. Comparative whole exome sequencing analysis of lesional and paired control tissues was conducted to identify genetic mutations in GCDF. Three of the six cases (50%) of GCDF harbored mutations in V-ATPase component genes, including ATP6AP1, ATP6V0C, and ATP6AP2. These findings expand the spectrum of tumors associated with V-ATPase mutations. It is important for dermatopathologists to be aware of clinical, histopathological, and molecular findings in GCDF, and to differentiate these from atypical or malignant GCT, as GCDF are benign and do not need aggressive surgical management. - Source: PubMed
Publication date: 2026/05/11
Jiang XingyuanHu RonghuaChoate Keith APanse Gauri