| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 1/20-1/50 | Human,Mouse,Rat |
| IHC | 1/100-1/200 | 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 | C1 esterase; C1S;;C1S |
| WB Predicted band size | Calculated MW: 77 kDa ; Observed MW: 90 kDa |
| 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 | A synthesized peptide derived from human C1S |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.05% BSA and 50% glycerol. |
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以下是3篇与C1s抗体相关的文献示例(内容为示例性概括，非真实文献)：
1. **"Targeting C1s in Hereditary Angioedema: A Monoclonal Antibody Approach"**
*作者：Suzuki et al. (2023)*
**摘要**：研究开发了一种靶向补体C1s的单克隆抗体，通过抑制其蛋白酶活性阻断经典补体通路，在动物模型中显著减少血管性水肿发作，为遗传性血管性水肿(HAE)提供潜在治疗策略。
2. **"Structural Insights into C1s Inhibition by Therapeutic Antibodies"**
*作者：Zhang et al. (2021)*
**摘要**：通过X射线晶体学解析C1s与抑制性抗体的复合物结构，揭示了抗体结合表位及抑制机制，为优化靶向C1s的抗体药物设计提供结构基础。
3. **"Anti-C1s Antibody Attenuates Inflammation in Systemic Lupus Erythematosus Models"**
*作者：Thompson et al. (2020)*
**摘要**：在SLE小鼠模型中，抗C1s抗体通过选择性抑制经典补体通路激活，减少肾脏免疫复合物沉积和炎症损伤，表明其治疗自身免疫疾病的潜力。
4. **"A Novel C1s-Specific Antibody-Drug Conjugate for Complement-Driven Disorders"**
*作者：Müller-Eberstein et al. (2022)*
**摘要**：报道了一种C1s靶向抗体-药物偶联物(ADC)，在体外和体内模型中展示出对补体过度激活相关疾病(如年龄相关性黄斑变性)的双重调控作用。
(注：以上为模拟内容，实际文献需通过PubMed/Google Scholar等平台检索确认。)
**Background of C1s Antibody**
C1s is a serine protease enzyme and a critical component of the complement system’s classical pathway. It forms a calcium-dependent complex with C1r and C1q within the C1 macromolecular complex. Upon binding of C1q to antigen-antibody complexes or other activators (e.g., apoptotic cells, pathogens), C1r undergoes autoactivation, subsequently cleaving and activating C1s. Active C1s then cleaves complement proteins C4 and C2. initiating the formation of C3 convertase (C4b2a), a key step in complement-mediated immune responses such as pathogen opsonization, inflammation, and cell lysis.
Dysregulation of C1s activity is linked to autoimmune and inflammatory diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis, due to excessive complement activation. Therapeutic C1s-targeting antibodies, often monoclonal, inhibit its proteolytic function to suppress pathological complement activation. For example, sutimlimab, a humanized anti-C1s antibody, has shown efficacy in treating cold agglutinin disease by blocking C1s-mediated hemolysis.
C1s antibodies are also vital tools in research and diagnostics. They enable the study of complement pathway dynamics, quantification of C1s levels in diseases, and assessment of therapeutic efficacy. However, challenges remain in balancing targeted inhibition to avoid compromising innate immunity. Ongoing research aims to refine specificity and optimize clinical applications of C1s antibodies.
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