ATP6V1G3
- Known as:
- ATP6V1G3
- Catalog number:
- 002242A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP6V1G3
Related genes to: ATP6V1G3
- Gene:
- ATP6V1G3 NIH gene
- Name:
- ATPase H+ transporting V1 subunit G3
- Previous symbol:
- -
- Synonyms:
- ATP6G3, Vma10
- Chromosome:
- 1q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-09
- Date modifiied:
- 2016-10-05
Related products to: ATP6V1G3
anti-ATP6V1G3anti-ATP6V1G3anti-ATP6V1G3anti-ATP6V1G3 (3A5)anti-ATP6V1G3 (3A5)anti-ATP6V1G3 type: Primary antibodies host: MouseATP6G3,ATP6V1G3,Homo sapiens,Human,Vacuolar proton pump subunit G 3,V-ATPase 13 kDa subunit 3,V-ATPase subunit G 3,V-type proton ATPase subunit G 3Atp6g3,Atp6v1g3,Mouse,Mus musculus,Vacuolar proton pump subunit G 3,V-ATPase 13 kDa subunit 3,V-ATPase subunit G 3,V-type proton ATPase subunit G 3ATP6V1G1 Gene ATPase, H+ transporting, lysosomal 13kDa, V1 subunit G1ATP6V1G3 antibody Host RabbitATP6V1G3 (Human) Recombinant Protein (P01)ATP6V1G3 (Human) Recombinant Protein (P01)ATP6V1G3 (Human) Recombinant Protein (Q01)ATP6V1G3 (Human) Recombinant Protein (Q01)ATP6V1G3 293T Cell Transient Overexpression Lysate(Denatured) Related articles to: ATP6V1G3
- Adrenocortical oncocytoma is a rare adrenal tumor. We report a 59-year-old Japanese woman with a right adrenal mass. The resected specimen showed a well-defined, mahogany-brown tumor measuring 4.3 cm. Microscopically, the tumor scored 0 under both the Lin-Weiss-Bisceglia system and the reticulin algorithm, indicating benignity. Immunohistochemical analysis revealed that tumor cells were positive for mitochondria and negative for BSND and ATP6V1G3. Ultrastructural examination found no uniform mitochondria in the cytoplasm of the tumor cells. The oncocytoma in this case may share more characteristics with an adrenal cortical adenoma than with a renal oncocytoma. - Source: PubMed
Publication date: 2026/04/29
Tachibana MitsuhiroNakagawa HiromichiNozawa HayatoFukuzawa Shigeki - V-ATPases are a class of multi-subunit protein complexes that utilize energy derived from ATP hydrolysis for mediating H transport across cell membranes, which plays an important role in a range of life activities by acidifying the intracellular and extracellular environment. Variants of V-ATPase genes may lead to complete or partial loss of V-ATPase activity, which in turn may impair the ability of type A intercalated cells in renal tubules to pump H into the tubular lumen, ultimately resulting in the onset of autosomal recessive distal renal tubular acidosis (dRTA). With the rapid development of molecular techniques, ATP6V0A4 and ATP6V1B1 have now been identified as the pathogenic genes for dRTA. Moreover, animal and cell experiments have substantiated the implication of V-ATPase subunit genes including ATP6V1C2 and ATP6V1G3 in the development of dRTA, though clinical evidence is still limited. This article has reviewed recent progress on the genetic and molecular mechanisms of V-ATPase subunit gene variants which can lead to dRTA, which may shed light on the diagnosis and treatment of this disease. - Source: PubMed
Peng SiqiWu QianqianYang JunlanWang BinZhang Xiaoliang - Liver fibrosis is characterized by an excessive reparative response to various etiological factors, with the activated hepatic stellate cells (aHSCs) leading to extracellular matrix (ECM) accumulation. Senescence is a stable growth arrest, and the senescence of aHSCs is associated with the degradation of ECM and the regression of hepatic fibrosis, making it a promising approach for managing hepatic fibrosis. The role and specific mechanisms by which V-Type Proton ATPase Subunit G 3 (ATP6V1G3) influences senescence in activated HSCs during liver fibrosis remain unclear. Our preliminary results reveal upregulation of ATP6V1G3 in both human fibrotic livers and murine liver fibrosis models. Additionally, ATP6V1G3 inhibition induced senescence in aHSCs in vitro. Moreover, suppressing Notch1 reversed the senescence caused by ATP6V1G3 inhibition in HSCs. Thus, targeting ATP6V1G3, which appears to drive HSCs senescence through the Notch1 pathway, emerges as a potential therapeutic strategy for hepatic fibrosis. - Source: PubMed
Publication date: 2024/09/14
Xue Xiao-PeiSheng YuRen Qi-QiXu Shi-MengLi MinLiu Zhao-XiuLu Cui-Hua - The maintenance of plasma pH is critical for life in all organisms. The kidney plays a critical role in acid-base regulation in vertebrates by controlling the plasma concentration of bicarbonate. The receptor tyrosine kinase IRR (insulin receptor-related receptor) is expressed in renal β-intercalated cells and is involved in alkali sensing due to its ability to autophosphorylate under alkalization of extracellular medium (pH > 7.9). In mice with a knockout of the gene, which encodes for IRR, urinary bicarbonate secretion in response to alkali loading is impaired. The specific regulatory mechanisms in the kidney that are under the control of IRR remain unknown. To address this issue, we analyzed and compared the kidney transcriptomes of wild-type and knockout mice under basal or bicarbonate-loaded conditions. Transcriptomic analyses revealed a differential regulation of a number of genes in the kidney. Using TaqMan real-time PCR, we confirmed different expressions of the , , , , , , , , and genes in IRR knockout mice. Also, we found that the expression of the gene is increased in wild-type mice after bicarbonate loading but not in knockout mice. Gene set enrichment analysis between the IRR knockout and wild-type samples identified that knockout causes alterations in expression of genes related mostly to the ATP metabolic and electron transport chain processes. - Source: PubMed
Publication date: 2023/12/04
Gantsova E ASerova O VEladari DBobrovskiy D MPetrenko A GElchaninov A VDeyev I E - Kidney intercalated cells (ICs) maintain acid-base homeostasis and recent studies have demonstrated that they function in the kidney's innate defense. To study kidney innate immune function, ICs have been enriched using vacuolar ATPase (V-ATPase) B1 subunit ()-Cre (B1-Cre) mice. Although is considered kidney specific, it is expressed in multiple organ systems, both in mice and humans, raising the possibility of off-target effects when using the Cre-lox system. We have recently shown using single-cell RNA sequencing that the gene that codes for the V-ATPase G3 subunit (mouse gene: ; human gene: ; protein abbreviation: G3) mRNA is selectively enriched in human kidney ICs. In this study, we generated -Cre (G3-Cre) reporter mice using CRISPR/CAS technology and crossed them with mice. The resultant G3-CreTdt progeny was evaluated for kidney specificity in multiple tissues and found to be highly specific to kidney cells with minimal or no expression in other organs evaluated compared with B1-Cre mice. Tdt cells were flow sorted and were enriched for IC marker genes on RT-PCR analysis. Next, we crossed these mice to ihCD59 mice to generate an IC depletion mouse model (G3-CreihCD59). ICs were depleted in these mice using intermedilysin, which resulted in lower blood pH, suggestive of a distal renal tubular acidosis phenotype. The G3-Cre mice were healthy, bred normally, and produce regular-sized litter. Thus, this new "IC reporter" mice can be a useful tool to study ICs. This study details the development, validation, and experimental use of a new mouse model to study the collecting duct and intercalated cells. Kidney intercalated cells are a cell type increasingly recognized to be important in several human diseases including kidney infections, acid-base disorders, and acute kidney injury. - Source: PubMed
Publication date: 2023/10/12
Saxena VijayArregui SamuelZhang ShaoboCanas JorgeQin XuebinHains David SSchwaderer Andrew L