| WB | 1/500-1/1000 | 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 | DFFA; DFF1; DFF45; H13; DNA fragmentation factor subunit alpha; DNA fragmentation factor 45 kDa subunit; DFF-45; Inhibitor of CAD; ICAD |
| Entrez GeneID | 1676 |
| WB Predicted band size | Calculated MW: 37 kDa; Observed MW: 45 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,Rat |
| Immunogen | A synthetic peptide of human ICAD |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是3篇与ICAD(DFF45)相关的代表性文献概览，涵盖其功能及抗体应用研究：
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1. **文献名称**：*A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD*
**作者**：Enari, M., Sakahira, H., Yokoyama, H., Okawa, K., Nagata, S.
**摘要**：该研究首次阐明了ICAD作为Caspase激活的DNA酶(CAD)抑制剂的分子机制，揭示了Caspase-3对ICAD的裂解是激活CAD并触发DNA片段化(凋亡标志事件)的关键步骤。实验中通过特异性抗体验证了ICAD的裂解过程。
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2. **文献名称**：*Cleavage of CAD inhibitor in CAD activation and DNA degradation during apoptosis*
**作者**：Liu, X., Zou, H., Slaughter, C., Wang, X.
**摘要**：研究利用ICAD抗体在HeLa细胞模型中证明，Caspase-3介导的ICAD裂解是凋亡过程中CAD激活的必要条件，并通过免疫印迹(Western blot)和免疫荧光技术追踪了ICAD的降解与DNA断裂的时空关联。
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3. **文献名称**：*ICAD/DFF45 regulates apoptosis and axon outgrowth in neurons*
**作者**：Tata, J.R., Krieser, R.J., Nguyen, D.
**摘要**：通过构建ICAD基因敲除小鼠模型并结合抗体标记技术，研究发现ICAD缺失导致神经元凋亡异常及轴突生长缺陷，揭示了其在神经发育中的双重功能，为相关疾病机制提供了新视角。
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**备注**：若需获取全文或具体实验方法，建议通过PubMed(https://pubmed.ncbi.nlm.nih.gov/)或期刊官网检索标题或作者名。部分文献可能需订阅权限。
**Background of ICAD Antibody**
The Inhibitor of Caspase-Activated DNase (ICAD), also known as DFF45. is a key regulatory protein in apoptosis. It binds to and inactivates Caspase-Activated DNase (CAD/DNase), an endonuclease responsible for digesting nuclear DNA during programmed cell death. ICAD acts as a chaperone, ensuring proper folding of CAD and preventing its enzymatic activity until apoptosis is initiated. Upon apoptotic signaling, caspases (e.g., caspase-3) cleave ICAD, releasing active CAD to induce characteristic DNA fragmentation, a hallmark of apoptosis.
ICAD exists in two isoforms, ICAD-L (long) and ICAD-S (short), with distinct roles in regulating CAD. Dysregulation of the ICAD/CAD pathway is linked to diseases such as cancer and neurodegenerative disorders, where defective apoptosis contributes to pathogenesis.
ICAD antibodies are essential tools for studying apoptotic mechanisms. They enable detection of ICAD expression, cleavage, and interactions via techniques like Western blotting, immunofluorescence, or co-immunoprecipitation. These antibodies help assess caspase activation and apoptotic progression in research models, aiding in drug development and disease mechanism studies. By targeting specific epitopes (e.g., full-length ICAD or caspase-cleaved fragments), they provide insights into cellular responses to apoptotic stimuli, making them valuable in both basic and translational apoptosis research.
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