ATP6V1D
- Known as:
- ATP6V1D
- Catalog number:
- 002233A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP6V1D
Related genes to: ATP6V1D
- Gene:
- ATP6V1D NIH gene
- Name:
- ATPase H+ transporting V1 subunit D
- Previous symbol:
- ATP6M
- Synonyms:
- VATD, VMA8
- Chromosome:
- 14q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-01
- Date modifiied:
- 2016-10-05
Related products to: ATP6V1D
anti-ATP6V1Danti-ATP6V1Danti-ATP6V1D (3G4)anti-ATP6V1D (3G4)anti-ATP6V1D (3G4)anti-ATP6V1D (3G4) type: Primary antibodies host: MouseAnti-ATP6V1D (3G4), Mouse Monoclonal to ATP6V1D, Isotype IgG2a, Host Mouseanti-ATP6V1D type: Primary antibodies host: MouseATP6M,ATP6V1D,Bos taurus,Bovine,Vacuolar proton pump subunit D,VATD,V-ATPase 28 kDa accessory protein,V-ATPase subunit D,V-type proton ATPase subunit DATP6M,ATP6V1D,Homo sapiens,Human,Vacuolar proton pump subunit D,VATD,V-ATPase 28 kDa accessory protein,V-ATPase subunit D,V-type proton ATPase subunit DAtp6m,Atp6v1d,Mouse,Mus musculus,Vacuolar proton pump subunit D,Vatd,V-ATPase 28 kDa accessory protein,V-ATPase subunit D,V-type proton ATPase subunit DATP6M,ATP6V1D,Oryctolagus cuniculus,Rabbit,Vacuolar proton pump subunit D,VATD,V-ATPase 28 kDa accessory protein,V-ATPase subunit D,V-type proton ATPase subunit DATP6V1C1 Gene ATPase, H+ transporting, lysosomal 42kDa, V1 subunit C1ATP6V1D antibody Host RabbitATP6V1D antibody Host Rabbit Related articles to: ATP6V1D
- Stroke is a major complication of atrial fibrillation (AF), and risk prediction using the congestive heart failure, hypertension, age, diabetes, stroke, vascular disease, and sex category score (CHA₂DS₂-VASc) remains limited by residual heterogeneity. We aimed to identify plasma proteins associated with post-AF stroke and evaluate whether a protein score provides incremental predictive information beyond CHA₂DS₂-VASc. - Source: PubMed
Publication date: 2026/07/23
Huang ShengkangFeng XinWu HuilinLiang RongxuanGao YuanWang ZhaojunTang BotaoWu JiatongFang JunkaiYang ZiangTiemuerniyazi XierailiLin JianchengDuan YijingxuanXu WenruMao HuaZhao WeiHu ZhanDuan ChuanzhiFeng Wei - is an obligate intracellular zoonotic protozoan parasite that can cause severe neonatal disease in congenitally acquired infections and severe opportunistic illnesses in immunocompromised individuals. Intracellularly, evades host cell defense mechanisms by residing within a specialized non-fusogenic membranous compartment known as the parasitophorous vacuole (PV). Notwithstanding this, we have previously shown that upregulation of small GTPase immunity-associated proteins (GIMAPs) during infection promotes fusion of lysosomes with the PV membrane (PVM), resulting in restriction of parasite replication in the -refractory Lewis (LEW) rat. Herein, we found that, in addition to GIMAPs, the LEW rat upregulates ATP6V1D, a subunit of the lysosomal vacuolar-type H+-ATPase (v-ATPase) proton pump, in response to infection. Disruption of ATP6V1D by CRISPR/Cas9 in a rat macrophage (NR8383) cell line impaired v-ATPase function, leading to defective lysosomal acidification and a concomitant increase in intracellular growth. Intriguingly, overexpression of GIMAP 5 or 6 transgene in the ∆ mutant cell line reduced parasite growth by 2.5- and 5-fold, respectively. Comparatively, overexpression of GIMAP 5 or 6 transgene in the wild-type NR8383 cell line had at least threefold more robust effect of reducing parasite growth than in the ∆ mutant cell. Together, our findings imply that while GIMAP-induced activation of lysosome translocation to the PVM is important for restricting parasite growth, concomitant upregulation of the ATP6V1D plays an additively significant role through enhanced acidification of lysosomes to activate hydrolytic enzymes that degrade the parasites following PVM fusion.IMPORTANCE is a highly prevalent parasite that causes severe illnesses in congenitally infected neonates and in immunocompromised individuals. No completely effective drugs nor vaccines exist against . Thus, understanding innate mechanisms that resistant hosts employ to orchestrate defenses against the parasite could unveil new strategies for control of toxoplasmosis. Herein, we analyzed transcriptomic data of the -resistant rat (Lewis) and identified small GTPase immunity-associated proteins (GIMAPs), and lysosome-associated proteins (including ATP6V1D) that are upregulated in response to infection. We investigated the interplay between those proteins and found that upregulated expression of GIMAPs drives lysosomes to fuse with the parasite vacuole, while upregulated ATP6V1D facilitates lysosomal acidification, which is important for activation of degradative lysosomal enzymes. Those events culminated in the restriction of intracellular growth. Collectively, our findings indicate that upregulation of GIMAPs and ATP6V1D orchestrates synergistic mechanisms that contribute to inhibition of intracellular growth. - Source: PubMed
Publication date: 2026/04/13
Mia Md MuktharKhan Shahbaz MAzam Abdur RehmanReilly JordanWitola William H - Pharmacodynamic biomarkers of sirolimus were investigated using omics analysis of tear fluids from Japanese patients with meibomian gland dysfunction (MGD). - Source: PubMed
Publication date: 2026/03/27
Zhou LeiShimizu HiroyukiTogashi YukiKirihara TomokoYang YuhanLam Chuen ThomasShimada HisaoTong Louis - The impact of metabolism-related genes on inflammatory bowel disease remains unclear. This study aimed to identify the causal relationships between metabolism-related genes and inflammatory bowel disease. - Source: PubMed
Publication date: 2026/01/22
Zhou HanXie KexinAn HongjinFeng YueYuan YifanGan Huatian - 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