| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Vacuolar proton pump subunit H; EC 3.6.3.14; V-ATPase subunit H; V-ATPase 50/57 kDa subunits; Vacuolar proton pump subunit SFD |
| Entrez GeneID | 51606; |
| WB Predicted band size | 55kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human |
| Immunogen | Synthesized peptide derived from internal of human ATP6V1H. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是3-4条关于ATP6V1H抗体的虚构参考文献示例(基于知识截止前的研究方向，实际文献需通过数据库验证)：
1. **文献名称**: *"ATP6V1H deficiency impairs osteoclast function and causes autosomal recessive osteoporosis"*
**作者**: Smith A, et al.
**摘要**: 研究通过ATP6V1H抗体检测发现，ATP6V1H基因缺陷小鼠模型中，破骨细胞V-ATP酶组装异常，导致溶酶体酸化障碍和骨吸收功能下降，揭示了该亚基在骨代谢中的关键作用。
2. **文献名称**: *"ATP6V1H as a potential biomarker in prostate cancer progression"*
**作者**: Lee B, et al.
**摘要**: 使用ATP6V1H特异性抗体进行免疫组化分析，发现前列腺癌组织中ATP6V1H表达上调，且与肿瘤转移和化疗耐药性相关，提示其作为治疗靶点的潜力。
3. **文献名称**: *"V-ATPase subunit ATP6V1H regulates lysosomal pH and autophagy in neurodegenerative disorders"*
**作者**: Chen X, et al.
**摘要**: 通过Western blot和免疫荧光(ATP6V1H抗体验证)，证实ATP6V1H缺失导致溶酶体pH失衡，阻碍自噬体降解，加剧阿尔茨海默模型小鼠的神经元损伤。
4. **文献名称**: *"Structural insights into the human V-ATPase: Cryo-EM analysis of ATP6V1H interactions"*
**作者**: Johnson R, et al.
**摘要**: 结合ATP6V1H抗体的免疫沉淀技术，解析了V-ATP酶中ATP6V1H亚基与其他组分的结合界面，为设计靶向V-ATP酶的药物提供结构基础。
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注：以上为模拟内容，实际文献需通过PubMed/Google Scholar检索关键词(如"ATP6V1H antibody"+"V-ATPase"+"disease model")。
The ATP6V1H antibody targets the ATP6V1H protein, a key subunit of the vacuolar-type H+-ATPase (V-ATPase) complex, which regulates intracellular pH by pumping protons across membranes. V-ATPases are multisubunit enzymes critical for acidifying organelles like lysosomes, endosomes, and secretory vesicles, influencing processes such as protein degradation, membrane trafficking, and ion homeostasis. The ATP6V1H subunit, part of the peripheral V1 domain, contributes to ATP hydrolysis and structural stability of the complex. Dysregulation of V-ATPase activity is linked to diseases including osteoporosis, renal tubular acidosis, and cancer metastasis.
ATP6V1H antibodies are essential tools for studying the expression, localization, and function of this subunit in cellular and disease models. They enable detection via techniques like Western blotting, immunofluorescence, and immunohistochemistry, aiding research into V-ATPase-related pathways. Studies using these antibodies have highlighted ATP6V1H's role in bone resorption, neurodevelopment, and tumor microenvironment modulation. Additionally, ATP6V1H variants are associated with genetic disorders, emphasizing its biomedical relevance.
These antibodies are validated for specificity across species, supporting translational research in metabolism, autophagy, and pH-dependent signaling. Their application helps unravel mechanisms underlying V-ATPase dysfunction in pathology and potential therapeutic targeting.
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