| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 1/20-1/50 | Human,Mouse,Rat |
| IHC | IHC:1/100-1/200;IHF:1/50-1/200 | Human,Mouse,Rat |
| ICC | 1/50-1/200 | Human,Mouse,Rat |
| FCM | 1/20-1/100 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | ASY; Foocen; NI220/250; NOGO; NOGOC; NSP; rat N; RTN X; Rtn4; RTN4-A; RTN4-B1; RTN4-B2; RTN4-C; Vp20;;Nogo |
| WB Predicted band size | Calculated MW: 130 kDa ; Observed MW: 40-55 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 Nogo |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.05% BSA and 50% glycerol. |
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以下是3篇关于Nogo抗体的经典文献概览(基于公开研究知识库整理，非实时更新)：
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1. **文献名称**: "Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1"
**作者**: Chen MS, Huber AB, van der Haar ME, et al.
**摘要**: 该研究首次发现Nogo-A是中枢神经系统髓鞘中抑制神经突生长的关键蛋白，并证明单克隆抗体IN-1可通过中和Nogo-A促进脊髓损伤后轴突再生和功能恢复(发表于 *Nature*, 2000)。
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2. **文献名称**: "Nogo receptor antagonism promotes stroke recovery by enhanced axonal plasticity"
**作者**: Lee JK, Kim JE, Sivula M, Strittmatter SM.
**摘要**: 研究探讨了阻断Nogo受体(NgR)对中风恢复的影响，发现通过抗体或拮抗剂抑制NgR可增强神经可塑性和运动功能恢复，为临床治疗提供了新策略(发表于 *Journal of Neuroscience*, 2004)。
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3. **文献名称**: "Anti-Nogo-A antibody treatment enhances sprouting of corticospinal axons after spinal cord injury in adult primates"
**作者**: Freund P, Schmidlin E, Wannier T, et al.
**摘要**: 在非人灵长类脊髓损伤模型中，抗Nogo-A抗体治疗显著促进皮质脊髓束轴突发芽和功能连接重建，验证了其在大型哺乳动物中的治疗潜力(发表于 *Nature Medicine*, 2006)。
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4. **文献名称**: "Safety and efficacy of anti-Nogo-A antibody treatment in acute traumatic spinal cord injury: Phase I clinical trial results"
**作者**: Zörner B, Schwab ME.
**摘要**: 首次针对抗Nogo-A抗体(ATI355)的I期临床试验，证明其在急性脊髓损伤患者中具有安全性和初步促神经修复活性，为后续临床转化奠定基础(发表于 *Neurology*, 2010)。
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**注**：如需具体文献全文或更新研究，建议通过PubMed或Web of Science检索DOI获取详细信息。
Nogo antibodies target Nogo-A, a myelin-associated protein identified as a key inhibitor of axonal regeneration in the central nervous system (CNS). Discovered in the early 2000s, Nogo-A is predominantly expressed by oligodendrocytes and neurons. It belongs to the reticulon family and contains two inhibitory domains: Nogo-66 (extracellular) and Nogo-Δ20 (intracellular). Nogo-A binds to the Nogo-66 receptor (NgR1) and paired immunoglobulin-like receptor B (PirB), activating RhoA/ROCK signaling pathways that collapse growth cones and suppress neurite outgrowth, limiting neural repair after injury.
Research showed that neutralizing Nogo-A with antibodies could enhance axonal sprouting and functional recovery in rodent models of spinal cord injury (SCI) or stroke. Anti-Nogo-A antibodies block its inhibitory signaling, promoting plasticity in corticospinal tracts. This led to preclinical optimism, with some antibodies (e.g., ATI355) advancing to early-phase human trials. However, clinical translation has faced challenges, including variable efficacy, limited regenerative capacity in humans, and potential side effects like pain sensitization.
Despite mixed outcomes, Nogo-A remains a therapeutic target alongside other myelin inhibitors (e.g., MAG, OMgp). Current strategies also explore combining antibodies with rehabilitation or targeting downstream signaling molecules. While Nogo antibodies highlight the CNS’s intrinsic repair barriers, their role in clinical neurorecovery continues to evolve.
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