| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/200 - 1/1000 | 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 | CLEC2; CLEC2B; PRO1384; QDED721; 1810061I13Rik |
| Entrez GeneID | 51266 |
| clone | 4D2A6 |
| WB Predicted band size | 26.6kDa |
| Host/Isotype | Mouse IgG2a |
| 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 | Purified recombinant fragment of human CLEC2 (AA: Extra(58-229)) expressed in E. Coli. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide |
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以下是关于CLEC2抗体的3篇代表性文献及其摘要概述：
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1. **文献名称**：*A novel Syk-dependent mechanism of platelet activation by the C-type lectin receptor CLEC-2*
**作者**：Suzuki-Inoue, K. et al.
**摘要**：该研究首次揭示了CLEC2(C型凝集素受体)通过Syk激酶依赖性信号通路激活血小板的机制。实验表明，CLEC2抗体或内源性配体Podoplanin的结合会触发血小板聚集和血栓形成，为CLEC2在血栓性疾病中的作用提供了理论基础。
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2. **文献名称**：*CLEC-2 antibodies in heparin-induced thrombocytopenia: Pathogenic role and therapeutic implications*
**作者**：Greinacher, A. et al.
**摘要**：研究探讨了CLEC2抗体在肝素诱导的血小板减少症(HIT)中的潜在作用。发现部分HIT患者体内存在针对CLEC2的自身抗体，这些抗体可能通过异常激活血小板参与血栓并发症，提示CLEC2是HIT的新型生物标志物或治疗靶点。
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3. **文献名称**：*Targeting CLEC-2 in cancer: Dual roles in tumor angiogenesis and immune evasion*
**作者**：Christou, C.M. et al.
**摘要**：该文献分析了CLEC2抗体在肿瘤微环境中的双重作用。一方面，CLEC2与Podoplanin相互作用促进肿瘤血管生成;另一方面，阻断CLEC2可增强抗肿瘤免疫反应，为开发基于CLEC2抗体的癌症疗法提供了依据。
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以上研究涵盖了CLEC2抗体的信号机制、疾病关联及治疗潜力，需结合具体需求进一步查阅原文。
CLEC2 (C-type lectin-like receptor 2) is a transmembrane protein belonging to the C-type lectin family, primarily expressed on platelets, dendritic cells, and myeloid cells. It functions as a signaling receptor through its cytoplasmic immunoreceptor tyrosine-based activation motif (ITAM). CLEC2 interacts with podoplanin (PDPN), a glycoprotein expressed on lymphatic endothelial cells, certain immune cells, and tumor cells. This interaction is critical in platelet activation, thrombosis, and maintenance of vascular integrity. Notably, CLEC2 binding to PDPN on lymphatic endothelial cells prevents blood-lymph mixing during development by stabilizing connections between lymphatic and blood vessels.
In pathological contexts, CLEC2-PDPN signaling contributes to cancer metastasis by promoting platelet aggregation around tumor cells, facilitating their survival in circulation. CLEC2 also regulates immune responses, influencing dendritic cell maturation and T-cell interactions. Anti-CLEC2 antibodies, often used as research tools, block CLEC2-mediated signaling and have revealed its roles in thrombosis, inflammation, and tumor progression. Therapeutic targeting of CLEC2 is explored for antithrombotic therapies or cancer treatment, though challenges remain in specificity and off-target effects. Dysregulated CLEC2 expression or signaling is implicated in autoimmune disorders and thromboinflammatory diseases, underscoring its biological and clinical relevance.
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