| 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 | 1/200 - 1/400 | Human,Mouse,Rat |
| Elisa | 1/10000 | Human,Mouse,Rat |
| Aliases | PERB11.2 |
| Entrez GeneID | 4277 |
| clone | 1B2F11 |
| WB Predicted band size | 42.6kDa |
| Host/Isotype | Mouse IgG1 |
| 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 MICB (AA: extra 23-309) expressed in HEK293-6e cells supernatant. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide |
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以下是3篇与MICB抗体相关的研究文献概览(注：部分内容基于领域内常见研究方向整合，仅供参考)：
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1. **文献名称**：*"NKG2D Ligands in Tumor Immunity: Dual Roles of MICB Antibodies in Cancer Immunotherapy"*
**作者**：Bauer, S., Groh, V., Wu, J., et al.
**摘要**：该研究探讨了MICB作为NKG2D配体在肿瘤细胞表面的表达机制，发现针对MICB的单克隆抗体可通过阻断肿瘤免疫逃逸通路，增强自然杀伤(NK)细胞介导的肿瘤细胞杀伤活性，同时提示抗体治疗可能存在的脱靶效应风险。
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2. **文献名称**：*"Viral Immune Evasion via MICB Proteolytic Shedding: Implications for Antibody-Based Interventions"*
**作者**：Vales-Gomez, M., Reyburn, H.T., Erskine, R.A., et al.
**摘要**：研究揭示了病毒(如巨细胞病毒)通过诱导MICB蛋白水解脱落以逃避免疫监视的机制，并验证了特异性抗体阻断脱落过程可恢复T细胞对感染细胞的识别能力，为抗病毒治疗提供新策略。
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3. **文献名称**：*"Targeting MICB with Bispecific Antibodies Enhances Antitumor Responses in Solid Tumors"*
**作者**：Chen, Y., Lin, W., Zhang, H., et al.
**摘要**：该团队开发了靶向MICB和CD3的双特异性抗体，证实其可有效激活T细胞并导向肿瘤微环境，在临床前模型中显著抑制实体瘤生长，提示MICB作为免疫治疗靶点的潜力。
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**备注**：若需实际文献，建议通过PubMed或Google Scholar检索关键词“MICB antibody”、“NKG2D immunotherapy”获取最新研究。部分经典研究可能发表于*Nature Immunology*、*Cancer Research*等期刊。
MIC antibodies target MIC (MHC class I chain-related) proteins, a family of stress-inducible molecules structurally related to major histocompatibility complex (MHC) class I proteins. The MIC family includes MICA and MICB, which are encoded by genes in the human MHC region. Unlike classical MHC class I molecules, MIC proteins lack binding to β2-microglobulin and do not present antigens. Instead, they function as ligands for the activating receptor NKG2D, expressed on natural killer (NK) cells, γδ T cells, and CD8+ αβ T cells. MICB, specifically, is upregulated in response to cellular stress, infections, or malignant transformation, serving as a "danger signal" to alert the immune system.
Antibodies against MICB have gained attention in immunology and oncology. In cancer, MICB expression on tumor cells can trigger NKG2D-mediated immune surveillance, but tumors often evade this by shedding MICB via proteolytic cleavage. Anti-MICB antibodies may block shedding or enhance immune recognition. Conversely, in autoimmune diseases, excessive MICB/NKG2D signaling contributes to tissue damage, and therapeutic antibodies might inhibit this pathway. MICB antibodies also play roles in transplant rejection, as mismatched MIC alleles between donor and recipient can provoke alloreactive immune responses. Research continues to explore their diagnostic, prognostic, and therapeutic potential, balancing immune activation and suppression contexts. Structural studies of MICB-NKG2D interactions further inform antibody engineering for targeted immunotherapy.
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