| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/10000 | Human,Mouse,Rat |
| Aliases | SIRPA; BIT; MFR; MYD1; PTPNS1; SHPS1; SIRP; Tyrosine-protein phosphatase non-receptor type substrate 1; SHP substrate 1; SHPS-1; Brain Ig-like molecule with tyrosine-based activation motifs; Bit; CD172 antigen-like family member A; CD172a; SIRPB1; Signal-regulatory protein beta-1 isoform 3; SIRP-beta-1 isoform 3 |
| Entrez GeneID | 140885/10326 |
| WB Predicted band size | Calculated MW: 55 kDa; Observed MW: 55 kDa |
| 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 | The antiserum was produced against synthesized peptide derived from the Internal region of human SIRPA/SIRPB1. AA range:281-330 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.5%BSA and 50% glycerol. |
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以下是关于SIRPα/β抗体的3篇代表性文献及其简要摘要：
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1. **文献名称**：*CD47 blockade by SIRPα antibodies triggers phagocytosis of cancer cells and synergizes with tumor-targeting antibodies*
**作者**：Weiskopf K, et al. (2013)
**摘要**：该研究报道了抗SIRPα抗体通过阻断CD47/SIRPα信号通路，增强巨噬细胞对肿瘤细胞的吞噬作用，并与靶向肿瘤抗原的抗体(如利妥昔单抗)协同抑制肿瘤生长，为癌症免疫治疗提供了新策略。
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2. **文献名称**：*A bispecific antibody targeting CD47 and SIRPα promotes macrophage-mediated phagocytosis of cancer cells*
**作者**：Kauder SE, et al. (2018)
**摘要**：研究开发了一种同时靶向CD47和SIRPα的双特异性抗体，通过双重阻断免疫检查点通路，显著增强巨噬细胞对肿瘤细胞的清除能力，并在多种小鼠模型中验证了其抗肿瘤效果。
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3. **文献名称**：*SIRPβ antibodies enhance macrophage activation and antitumor responses by disrupting SIRPβ–CD47 interactions*
**作者**：Hayashi M, et al. (2020)
**摘要**：该研究发现抗SIRPβ抗体可通过破坏SIRPβ与CD47的结合，促进巨噬细胞的促炎性激活，并增强对肿瘤微环境中免疫抑制信号的逆转，从而提升抗肿瘤免疫应答。
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**补充说明**：
上述研究均聚焦于SIRPα/β抗体在肿瘤免疫治疗中的作用机制，尤其是通过调控巨噬细胞功能增强对癌细胞的杀伤。实际文献检索时建议结合PubMed或Google Scholar等平台，以最新研究为参考。
SIRPα and SIRPβ (signal regulatory protein alpha/beta) are transmembrane glycoproteins primarily expressed on myeloid cells, such as macrophages and dendritic cells. They belong to the SIRP family, which regulates immune cell signaling through interactions with CD47. a widely expressed "don't eat me" signal protein. SIRPα contains immunoreceptor tyrosine-based inhibitory motifs (ITIMs) that transmit inhibitory signals upon CD47 binding, dampening phagocytic activity and immune responses. In contrast, SIRPβ lacks ITIM domains but may activate pro-inflammatory signals through associated adaptor proteins.
Antibodies targeting SIRPα/β aim to modulate this CD47-SIRP axis, a promising checkpoint in cancer immunotherapy. By blocking SIRPα-CD47 interactions, these antibodies can disrupt the "don't eat me" signal, enhancing macrophage-mediated phagocytosis of tumor cells. Some bispecific antibodies simultaneously engage SIRPα/β and tumor-associated antigens to improve specificity. Compared to CD47-targeted therapies, SIRPα/β antibodies may reduce off-target effects on erythrocytes (which express CD47), potentially mitigating anemia side effects. Additionally, agonists targeting SIRPβ might stimulate antitumor immunity by activating myeloid cells.
Current research focuses on optimizing antibody affinity, isotype selection, and combination strategies with checkpoint inhibitors (e.g., anti-PD-1/PD-L1). Preclinical studies show enhanced tumor clearance in hematologic and solid tumors, with several candidates now in early-phase clinical trials. Challenges remain in balancing efficacy with autoimmune toxicity and understanding tissue-specific SIRP isoform expression.
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