| 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 | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | CRMP1, DPYSL1, CRMP-1, DRP-1, Dihydropyrimidinase-like 1, DRP1, ULIP3, Unc-33-like phosphoprotein 3, ULIP-3 |
| Entrez GeneID | 1400; |
| WB Predicted band size | 62kDa |
| 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,Mouse,Rat |
| Immunogen | A synthesized peptide derived from human CRMP-1 (Phospho-Tyr504) |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是基于CRMP-1 (Phospho-Tyr504)抗体相关研究的模拟参考文献示例。请注意，这些文献为假设性示例，实际引用时需通过学术数据库核实：
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1. **文献名称**: *"Tyrosine 504 phosphorylation of CRMP1 modulates axonal growth cone collapse through Semaphorin 3A signaling"*
**作者**: Arimura, N., et al.
**摘要**: 本研究探讨了Semaphorin 3A信号通路中CRMP1 Tyr504磷酸化的作用。通过使用Phospho-Tyr504特异性抗体，作者发现该位点的磷酸化介导生长锥塌陷，并影响CRMP1与微管蛋白的结合能力，揭示了其在神经元导向中的关键机制。
2. **文献名称**: *"Phosphorylation-dependent regulation of CRMP1 in Alzheimer’s disease models"*
**作者**: Hou, Y., et al.
**摘要**: 研究分析了阿尔茨海默病模型中CRMP1磷酸化异常与tau蛋白病理的关系。利用Phospho-Tyr504抗体，作者发现患者脑组织中Tyr504磷酸化水平显著升高，提示其可能作为神经退行性疾病的潜在生物标志物。
3. **文献名称**: *"Development and validation of a phospho-specific antibody for CRMP1 tyrosine 504 phosphorylation"*
**作者**: Smith, J., et al.
**摘要**: 该文献描述了CRMP1 (Phospho-Tyr504)抗体的制备与验证。通过点突变和肽竞争实验证实抗体特异性，并展示其在免疫印迹和免疫组化中的应用，为后续功能研究提供工具支持。
4. **文献名称**: *"CRMP1 phosphorylation at Tyr504 disrupts neuronal polarity via RhoA/ROCK pathway activation"*
**作者**: Yoshimura, T., et al.
**摘要**: 研究揭示了Tyr504磷酸化通过激活RhoA/ROCK通路破坏神经元极性。通过Phospho-Tyr504抗体的共聚焦成像，作者证明磷酸化CRMP1在轴突形成中的抑制作用，为神经发育障碍提供了机制解释。
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建议通过PubMed、Google Scholar或Web of Science检索关键词“CRMP1 Tyr504 phosphorylation antibody”或相关信号通路(如Semaphorin、Alzheimer’s disease)，以获取真实文献。抗体供应商(如CST、Abcam)的产品页面也可能提供引用文献列表。
CRMP-1 (Collapsin Response Mediator Protein-1), also known as DPYSL2. is a cytosolic phosphoprotein critical for neuronal development, including axon guidance, neurite outgrowth, and synaptic plasticity. Its activity is tightly regulated by phosphorylation, particularly at Tyr504. which modulates interactions with downstream signaling components. The Phospho-Tyr504 epitope reflects activation of the Semaphorin 3A (Sema3A) signaling pathway, where Sema3A binding to neuropilin/plexin receptors triggers kinase cascades (e.g., Fyn, Cdk5) that phosphorylate CRMP-1. This post-translational modification alters CRMP-1’s conformation, reducing its affinity for tubulin heterodimers and impairing microtubule assembly, ultimately influencing growth cone collapse or axon repulsion.
Antibodies targeting CRMP-1 (Phospho-Tyr504) are essential tools for studying neuronal signaling dynamics, neurodegenerative diseases (e.g., Alzheimer’s, where aberrant CRMP-1 phosphorylation correlates with tau pathology), and neurodevelopmental disorders. They enable detection of phosphorylation-dependent CRMP-1 localization or activity shifts via techniques like Western blotting, immunohistochemistry, or immunofluorescence. Research using these antibodies has also explored roles in non-neuronal contexts, including cancer metastasis and immune regulation, highlighting CRMP-1’s broad functional versatility. Proper validation (e.g., knockout controls, peptide competition) is critical due to potential cross-reactivity with homologous CRMP family members.
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