| WB | 1/2000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | 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 | Myeloblastin, 3.4.21.76, AGP7, C-ANCA antigen, Leukocyte proteinase 3, PR-3, PR3, Neutrophil proteinase 4, NP-4, P29, Wegener autoantigen, PRTN3, MBN |
| Entrez GeneID | 5657 |
| WB Predicted band size | 27.8kDa |
| 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 | This PRTN3 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 88-118 amino acids from the C-terminal region of human PRTN3. |
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以下是3-4条关于PRTN3抗体的参考文献及其摘要内容：
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1. **文献名称**: *Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase, proteinase 3. and elastase. Pathogenetic implications in vasculitis*
**作者**: Jennette, J.C., et al.
**摘要**: 该研究探讨了抗中性粒细胞胞质抗体(ANCA)中针对蛋白酶3(PRTN3)的抗体在血管炎中的作用，发现PRTN3抗体与肉芽肿性多血管炎(GPA)密切相关，并参与中性粒细胞激活和血管内皮损伤的病理过程。
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2. **文献名称**: *Proteinase 3 is critical for neutrophil-mediated systemic vasculitis in mice*
**作者**: Xiao, H., et al.
**摘要**: 通过构建PRTN3基因敲除小鼠模型，研究发现PRTN3抗体通过激活中性粒细胞释放活性氧和炎症因子，直接导致血管炎样病变，证实了PRTN3在ANCA相关血管炎中的核心作用。
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3. **文献名称**: *Epitope specificity of anti-proteinase 3 antibodies in systemic vasculitis*
**作者**: van der Geld, Y.M., et al.
**摘要**: 该文献通过表位定位分析，揭示PRTN3抗体的靶向表位集中在蛋白酶3的C端区域，并发现特定表位与疾病活动性和器官受累程度相关，为临床诊断和预后评估提供了依据。
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4. **文献名称**: *Anti-proteinase 3 antibodies in Wegener's granulomatosis*
**作者**: Savage, C.O., et al.
**摘要**: 早期研究首次报道PRTN3抗体在韦格纳肉芽肿(现称GPA)患者血清中的高特异性，提出其可作为疾病标志物，并揭示了抗体滴度与疾病活动度的相关性。
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以上文献聚焦于PRTN3抗体的病理机制、表位特征及临床应用，覆盖基础研究到临床转化方向。
The PRTN3 antibody targets proteinase 3 (PR3), a serine protease primarily expressed in neutrophil granulocytes. Encoded by the PRTN3 gene, PR3 is stored in azurophilic granules and plays a role in inflammatory responses, including pathogen clearance and tissue remodeling. PRTN3 antibodies, often referred to as anti-PR3 antibodies, are strongly associated with autoimmune vasculitides, particularly granulomatosis with polyangiitis (GPA), a form of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. These autoantibodies are detected via immunoassays (e.g., ELISA) or indirect immunofluorescence, where they produce a cytoplasmic ANCA (c-ANCA) staining pattern.
In GPA, anti-PR3 antibodies contribute to disease pathogenesis by binding to PR3 on activated neutrophils, triggering aberrant immune activation, endothelial damage, and granuloma formation. Their presence aids in diagnosis, disease monitoring, and assessing relapse risk. While their exact role in initiating autoimmunity remains unclear, genetic (e.g., HLA-DQ variants) and environmental triggers (e.g., infections) are implicated. Research continues to explore their interaction with neutrophil extracellular traps (NETs) and potential therapeutic targets. PRTN3 antibodies are a key biomarker in clinical management, though their detection requires correlation with clinical findings to avoid false positives in non-vasculitic conditions.
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