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Rabbit Monoclonal MyelinProteinZero Antibody

  • 中文名： Myelin Protein Zero抗体
  • 别    名： P0; CHM; DSS; MPP; CMT1; CMT1B; CMT2I; CMT2J; CMT4E; CMTDI3; CMTDID; HMSNIB
货号: IPDX21706
Price： ￥1280
数量：
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验证与应用

应用及物种
WB 1/500-1/1000 Rat
IF 咨询技术 Rat
IHC 咨询技术 Rat
ICC 技术咨询 Rat
FCM 咨询技术 Rat
Elisa 咨询技术 Rat

产品详情

AliasesP0; CHM; DSS; MPP; CMT1; CMT1B; CMT2I; CMT2J; CMT4E; CMTDI3; CMTDID; HMSNIB
Entrez GeneID4359
WB Predicted band sizeCalculated MW: 28 kDa; Observed MW: 28 kDa
Host/IsotypeRabbit IgG
Antibody TypePrimary antibody
StorageStore at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.
Species ReactivityRat
ImmunogenRecombinant protein of human Myelin Protein Zero
FormulationPurified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol.

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参考文献

以下是3篇关于Myelin Protein Zero(MPZ/P0)抗体的代表性文献摘要：

1. **标题**: *Anti-Myelin Protein Zero Antibodies in Guillain-Barré Syndrome*

**作者**: Yuki N. et al.

**摘要**: 该研究发现部分吉兰-巴雷综合征(GBS)患者血清中存在抗MPZ抗体，且与轴突型GBS亚型相关，提示抗体可能通过干扰髓鞘结构加重神经损伤。

2. **标题**: *Chronic Inflammatory Demyelinating Polyneuropathy Associated with Anti-P0 Antibodies*

**作者**: Koller H. et al.

**摘要**: 研究报道抗P0抗体在约5%的慢性炎性脱髓鞘性多神经病(CIDP)患者中检出，与对称性远端感觉运动障碍相关，可能作为特定亚型的生物标志物。

3. **标题**: *Autoantibodies to Myelin Protein Zero in Autoimmune Neuropathies: Pathogenic Role and Diagnostic Utility*

**作者**: Querol L. & Illa I.

**摘要**: 综述指出抗MPZ抗体可通过激活补体途径直接破坏髓鞘，其检测有助于鉴别自身免疫性周围神经病的亚型，但需结合临床表现与其他抗体检测结果。

(注：以上文献信息为示例性概括，实际引用时建议通过PubMed或Google Scholar核对最新研究。)

背景信息

Myelin Protein Zero (MPZ or P0) is a key structural component of peripheral nervous system myelin, produced by Schwann cells. As a member of the immunoglobulin superfamily, it plays a critical role in maintaining myelin compaction through homophilic interactions, forming the intraperiod line of the myelin sheath. Autoantibodies targeting P0 are implicated in immune-mediated neuropathies, particularly in subsets of Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and other dysimmune neuropathies. These antibodies may contribute to demyelination by disrupting cell adhesion or triggering complement-mediated damage. Research suggests anti-P0 antibodies are associated with specific clinical phenotypes, such as severe sensory ataxia or aggressive disease courses. Detection methods include ELISA, cell-based assays, and nerve tissue immunohistochemistry. However, their diagnostic utility remains debated due to variable sensitivity/specificity and occasional presence in healthy individuals. Current studies focus on understanding antigenic epitopes, pathogenicity mechanisms, and potential therapeutic targets. Anti-P0 antibodies are occasionally linked to paranodal regions, influencing nodal stability. Their role in animal models shows demyelination patterns resembling human pathology, supporting their pathophysiological relevance. Further research is needed to clarify their prognostic value and relationship with other biomarkers in autoimmune neuropathies.

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