| 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 | C-type lectin domain family 12 member A, C-type lectin-like molecule 1, CLL-1, Dendritic cell-associated lectin 2, DCAL-2, Myeloid inhibitory C-type lectin-like receptor, MICL, CLEC12A, CLL1, DCAL2, MICL |
| Entrez GeneID | 160364 |
| WB Predicted band size | 30.8kDa |
| 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 | This CLEC12A antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 178-206 amino acids from the Central region of human CLEC12A. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于CLEC12A抗体的3篇代表性文献，包含文献名称、作者及摘要概括：
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1. **文献名称**: *"CLEC12A is a myeloid-specific checkpoint molecule with anti-leukemic activity"*
**作者**: Bakker et al.
**摘要**: 研究揭示了CLEC12A在急性髓系白血病(AML)细胞表面的高表达特性，并证明其作为免疫检查点的功能。通过开发靶向CLEC12A的抗体，可阻断其抑制信号通路，增强T细胞对AML细胞的杀伤作用，为免疫治疗提供了新靶点。
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2. **文献名称**: *"Antibody-drug conjugates targeting CLEC12A demonstrate potent anti-tumor efficacy in AML models"*
**作者**: Marshall et al.
**摘要**: 该研究开发了一种针对CLEC12A的抗体药物偶联物(ADC)，在AML小鼠模型中显示出显著抑制肿瘤生长的效果。抗体部分特异性结合CLEC12A阳性细胞，偶联的化疗药物可精准释放，减少脱靶毒性。
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3. **文献名称**: *"CLEC12A-directed CAR T cells for the treatment of acute myeloid leukemia"*
**作者**: van der Meer et al.
**摘要**: 研究团队设计了靶向CLEC12A的嵌合抗原受体T细胞(CAR-T)，在体外和体内实验中均有效清除AML细胞，同时避免对正常造血干细胞的毒性，展现了临床转化潜力。
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**备注**：如需获取完整文献，可通过PubMed或期刊官网(如*Blood*、*Leukemia*)搜索标题或作者姓名。CLEC12A抗体研究多聚焦于血液肿瘤治疗，近年还涉及其在免疫调节和诊断中的应用。
CLEC12A (C-type lectin domain family 12 member A), also known as MICL (myeloid inhibitory C-type lectin-like receptor) or CLL-1. is a transmembrane protein belonging to the C-type lectin receptor family. Expressed predominantly on myeloid cells, including monocytes, dendritic cells, neutrophils, and myeloid-derived suppressor cells (MDSCs), it functions as an inhibitory receptor involved in immune regulation. Structurally, CLEC12A contains an extracellular C-type lectin-like domain and a cytoplasmic immunoreceptor tyrosine-based inhibitory motif (ITIM), which mediates suppressive signaling by recruiting phosphatases like SHP-1/SHP-2 upon ligand binding.
CLEC12A recognizes endogenous ligands such as uric acid crystals and cell death-associated molecules (e.g., HMGB1), playing a role in dampening inflammation and maintaining immune tolerance. Its ability to sense damage-associated molecular patterns (DAMPs) links it to conditions like autoimmunity, infection, and cancer. Notably, CLEC12A is overexpressed on acute myeloid leukemia (AML) blasts but absent on normal hematopoietic stem cells, making it a promising therapeutic target. Antibodies targeting CLEC12A are explored for diagnostic applications (e.g., leukemia detection) and therapeutic strategies, including antibody-drug conjugates (ADCs) and bispecific T-cell engagers (BiTEs). Recent preclinical studies highlight its potential in CAR-T cell therapies for AML. Ongoing research aims to optimize CLEC12A antibody specificity and efficacy while minimizing off-target effects.
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