ATP6V0A1
- Known as:
- ATP6V0A1
- Catalog number:
- 002246A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP6V0A1
Related genes to: ATP6V0A1
- Gene:
- ATP6V0A1 NIH gene
- Name:
- ATPase H+ transporting V0 subunit a1
- Previous symbol:
- VPP1, ATP6N1, ATP6N1A
- Synonyms:
- a1, Vph1, Stv1
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-03
- Date modifiied:
- 2016-10-05
Related products to: ATP6V0A1
anti-ATP6V0A1anti-ATP6V0A1anti-ATP6V0A1 type: Primary antibodies host: MouseATP6AP1L Gene ATPase, H+ transporting, lysosomal accessory protein 1-likeATP6N1,ATP6N1A,ATP6V0A1,Clathrin-coated vesicle_synaptic vesicle proton pump 116 kDa subunit,Homo sapiens,Human,Vacuolar adenosine triphosphatase subunit Ac116,Vacuolar proton pump subunit 1,VacuolarATP6N1,ATP6V0A1,Bos taurus,Bovine,Clathrin-coated vesicle_synaptic vesicle proton pump 116 kDa subunit,Vacuolar adenosine triphosphatase subunit Ac116,Vacuolar proton pump subunit 1,Vacuolar proton trAtp6n1,Atp6v0a1,Clathrin-coated vesicle_synaptic vesicle proton pump 116 kDa subunit,Mouse,Mus musculus,Vacuolar adenosine triphosphatase subunit Ac116,Vacuolar proton pump subunit 1,Vacuolar proton tAtp6n1,Atp6v0a1,Clathrin-coated vesicle_synaptic vesicle proton pump 116 kDa subunit,Rat,Rattus norvegicus,Vacuolar adenosine triphosphatase subunit Ac116,Vacuolar proton pump subunit 1,Vacuolar protoATP6V0A1 antibody Host rabbitATP6V0A1 (C-term) antibody Host rabbitATP6V0A1 (C-term) antibody Ab host: RabbitATP6V0A1 (Human) Recombinant Protein (P01)ATP6V0A1 (Human) Recombinant Protein (Q01)ATP6V0A1 3&_39;UTR Lenti-reporter-Luc VectorATP6V0A1 antibody Related articles to: ATP6V0A1
- Carbonic anhydrase 7 (CA7) is a zinc-containing metalloenzyme that catalyzes the reversible conversion between CO and HCO, playing a vital role in ion transport and acid-base balance in aquatic organisms thereby supplying essential substrates for osmoregulatory proteins. However, its molecular mechanism in crustacean adaptation to alkalinity stress remains elusive. In this study, EsCA7 from the Chinese mitten crab (Eriocheir sinensis) was characterized, revealing its conserved zinc-binding sites and cytoplasmic localization. Knockdown of EsCA7 by RNA interference both in vitro and in vivo significantly downregulated the expression of key ion transport genes, including ATP6V0A1, SLC9B2, CLCN7, and AQP4. This indicates the central role of EsCA7 in maintaining cellular ion homeostasis and acid-base balance. Furthermore, EsCA7 deficiency triggered electrolyte disturbance and oxidative stress. These changes may have enhanced the negative regulatory effect of SOCS3, thereby downregulating the anti-apoptotic gene BCL2 and upregulating CASP7. Cellular assays demonstrated that EsCA7 knockdown markedly increased mitochondrial-dependent apoptosis in hemocytes. Collectively, our findings reveal that EsCA7 is essential for maintaining ion homeostasis and mitigating oxidative stress-induced apoptosis, thereby elucidating a key molecular mechanism underlying alkalinity tolerance in E. sinensis. - Source: PubMed
Publication date: 2026/05/23
Ma JunleiFan ZihanBai YuqiLiang YidongYou LeiXu DongpoBai Yulin - Alzheimer's disease (AD) is a neurodegenerative disorder characterized by neuronal loss and cognitive deficiency. Mitochondrial dysfunction and lysosomal abnormalities are critical during AD pathogenesis. The vesicular ATPase (v-ATPase) is a core regulator of lysosomal function, and its dysfunction impairs iron-sulfur protein synthesis and mitochondrial function. In this study, 4-month-old amyloid precursor protein/presenilin 1 (APP/PS1) double transgenic mice were treated with alkaloids from Dendrobium nobile Lindl (DNLA) at 20 and 40 mg/kg/day via oral gavage for 5 months (n = 10 per group). The Y-maze test showed that DNLA alleviated cognitive dysfunction in APP/PS1 mice. HE, Nissl, and β-galactosidase staining indicated that DNLA mitigated brain damage. DNLA also increased the protein levels of v-ATPase subunits ATP6V1A and ATP6V0a1 in the cortex, promoted mitochondrial iron uptake and utilization, enhanced mitochondrial function, and reduced neuronal damage. Dendrobine (DDB) accounted for 84.6% in DNLA used for animal experiments, and purified DDB (99.7%) was applied for in vitro assays. In PC12 cells, DDB restored ATP6V1A expression, enhanced v-ATPase activity, delayed cellular senescence, improved iron utilization, and elevated mitochondrial membrane potential and ATP levels in ATP6V1A-knockdown cells. These findings suggest that DNLA may attenuate learning and memory impairment in APP/PS1 mice. The mechanism may be related to enhanced v-ATPase activity, promoted mitochondrial iron uptake and utilization, and improved mitochondrial function. - Source: PubMed
Publication date: 2026/05/22
Li QiyeYang YanGuo BinLiu XuejiaLuo GuohuiWu YajuanNie Jing - - Source: PubMed
Publication date: 2026/05/18
Gu JieRuan JiachengLi ZehuaFu HuilinShi QiangZhu JuanWu JinGong XunShi HaifengJiang Peng - Ryanodine receptors (RYRs) are ER-resident Ca-release channels enriched in excitable cells, including neurons. RYR hyperactivity is implicated in early pathogenesis of disorders such as Alzheimer's disease (AD), which is associated with impaired autophagy. We recently uncovered a mechanism linking RYR activity to lysosome availability for autophagy. RYRs localize to ER-lysosome contact sites via direct binding to ATP6V0A1, a V-ATPase subunit that also suppresses RYR-mediated Ca release. In human iPSC-derived cortical neurons, spontaneous RYR activity promotes lysosomal secretion, depleting the intracellular lysosomal pool and inhibiting autophagic flux. RYR inhibition promotes ERlysosome contacts, limits lysosomal secretion, and restores lysosome availability for autophagosome fusion and cargo degradation (including APP). Conversely, disrupting the RYR:ATP6V0A1 interaction using a RYR-derived protein fragment serving as a "decoy" for ATP6V0A1 evokes RYR hyperactivity and stimulates lysosomal secretion. In this Punctum, we discuss how this RYR2:ATP6V0A1 "contact-site hub" may be perturbed in disease and highlight open questions on how lysosomes decode RYR-derived Ca signals. - Source: PubMed
Publication date: 2026/05/14
Loncke JensCallens ManonBultynck GeertVervliet Tim - Variants in the ATP6V0A1 gene, which encodes the α1 subunit of the V0 domain of the V-ATPases, are associated with developmental and epileptic encephalopathy 104 (DEE104). This study aimed to characterize the clinical features of a Chinese patient with ATP6V0A1 variants and facilitate the early diagnosis and treatment. - Source: PubMed
Publication date: 2026/05/03
Peng LongyingWei CuijieZhang YuehuaZhang QingpingWang WenhuiBao Xinhua