| WB | 咨询技术 | 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 | 1/200 - 1/400 | Human,Mouse,Rat |
| Elisa | 1/10000 | Human,Mouse,Rat |
| Aliases | Fbxo32;MAFbx; Gm20361; AI430017; ATROGIN1; 4833442G10Rik |
| Entrez GeneID | 67731 |
| clone | 5C11D1 |
| WB Predicted band size | 41.5kDa |
| Host/Isotype | Rat IgG3 |
| 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 of human ATROGIN-1 (AA: 23-35). |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是3-4篇关于 **ATROGIN-1(MAFbx)抗体** 的参考文献及简要摘要：
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1. **文献名称**: *Identification of ubiquitin ligases required for skeletal muscle atrophy*
**作者**: Bodine, S.C., et al.
**摘要**: 该研究首次鉴定了ATROGIN-1(MAFbx)作为肌肉萎缩特异性泛素连接酶，通过在小鼠去神经和饥饿模型中利用特异性抗体检测其表达，证实其通过泛素-蛋白酶体途径促进肌肉蛋白降解。
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2. **文献名称**: *FOXO transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 (MAFbx) in skeletal muscle*
**作者**: Sandri, M., et al.
**摘要**: 研究揭示了FOXO转录因子在调控ATROGIN-1基因表达中的作用，通过Western blot和免疫组化(使用ATROGIN-1特异性抗体)证明其在肌肉萎缩中的关键调控机制。
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3. **文献名称**: *Cancer cachexia is regulated by selective targeting of skeletal muscle gene products*
**作者**: Cai, D., et al.
**摘要**: 文章探讨了癌症恶病质中骨骼肌萎缩的分子机制，利用ATROGIN-1抗体检测其在肿瘤模型中的表达上调，表明其与肌肉质量减少直接相关。
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4. **文献名称**: *Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases*
**作者**: Sacheck, J.M., et al.
**摘要**: 研究比较了不同肌肉萎缩模型中ATROGIN-1的表达差异，通过抗体检测证实其在糖皮质激素诱导和去神经萎缩中的特异性激活。
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以上文献均涉及ATROGIN-1抗体的应用(如Western blot、免疫组化)，并围绕其在肌肉萎缩机制中的功能展开。建议通过PubMed或期刊官网获取全文以验证细节。
The ATROGIN-1 antibody is a crucial tool for studying muscle atrophy and protein degradation pathways. ATROGIN-1. also known as MAFbx (Muscle Atrophy F-box), is an E3 ubiquitin ligase encoded by the *FBXO32* gene. It plays a central role in the ubiquitin-proteasome system (UPS), tagging specific substrates for degradation. Discovered in 2001. ATROGIN-1 gained attention due to its rapid upregulation during skeletal muscle atrophy triggered by conditions like fasting, denervation, disuse, or cancer cachexia. It works in tandem with MuRF1 (another E3 ligase), targeting key structural and regulatory proteins such as MyoD and eIF3-f for proteasomal breakdown, thereby promoting muscle loss.
Antibodies against ATROGIN-1 are widely used in research to detect protein expression levels in tissues or cell cultures, employing techniques like Western blotting, immunohistochemistry, and immunofluorescence. These reagents help elucidate mechanisms underlying muscle wasting in diseases (e.g., muscular dystrophy, cancer, sepsis) or age-related sarcopenia. Validation of ATROGIN-1 antibodies often involves testing in knockout models or atrophy-inducing conditions to confirm specificity. Beyond basic research, such antibodies hold potential for developing diagnostic biomarkers or therapeutic strategies to modulate UPS activity. However, variability in antibody performance across species or experimental setups requires careful optimization. Overall, ATROGIN-1 antibodies remain indispensable for exploring cellular proteostasis and muscle biology.
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