| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 1/20 | 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 | 咨询技术 | Human,Mouse,Rat |
| Aliases | BTK; AGMX1; ATK; BPK; Tyrosine-protein kinase BTK; Agammaglobulinaemia tyrosine kinase; ATK; B-cell progenitor kinase; BPK; Bruton tyrosine kinase |
| Entrez GeneID | 695 |
| WB Predicted band size | Calculated MW: 76 kDa; Observed MW: 76 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 | Recombinant protein of human BTK |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
+ +
以下是3篇关于BTK抑制剂的关键文献摘要(注：BTK相关研究以抑制剂为主，抗体研究较少，以下提供抑制剂领域的高影响力论文)：
---
1. **文献名称**：Ibrutinib as Initial Therapy for Patients with Chronic Lymphocytic Leukemia
**作者**：Byrd, J.C. et al.
**摘要**：该III期临床试验证实，BTK抑制剂依鲁替尼(Ibrutinib)作为慢性淋巴细胞白血病(CLL)的一线治疗方案，显著延长无进展生存期(PFS)和总生存期(OS)，且安全性优于传统化疗，奠定了BTK抑制剂在B细胞恶性肿瘤治疗中的地位。
2. **文献名称**：Acalabrutinib versus Ibrutinib in Relapsed/Refractory Chronic Lymphocytic Leukemia
**作者**：Byrd, J.C. et al.
**摘要**：研究对比第二代BTK抑制剂阿卡替尼(Acalabrutinib)与一代药物依鲁替尼的疗效和安全性，显示两者疗效相当，但阿卡替尼的心脏毒性更低，为优化BTK抑制剂的临床选择提供依据。
3. **文献名称**：Targeting BTK in B Cell Malignancies: From Mode of Action to Resistance Mechanisms
**作者**：Woyach, J.A. et al.
**摘要**：该综述系统总结了BTK在B细胞信号通路中的作用、抑制剂的作用机制及耐药性产生的原因(如BTK C481突变)，并探讨了克服耐药的策略，如开发非共价抑制剂(如Pirtobrutinib)。
4. **文献名称**：Combination of Rituximab and Ibrutinib in Waldenström’s Macroglobulinemia
**作者**：Treon, S.P. et al.
**摘要**：研究证明BTK抑制剂依鲁替尼联合抗CD20抗体利妥昔单抗可显著提高华氏巨球蛋白血症患者的总体缓解率，提示BTK抑制剂与单抗联用的协同潜力。
---
**备注**：若需BTK抗体(非抑制剂)相关文献，可进一步说明具体研究方向(如诊断抗体、治疗性抗体等)。
Bruton’s tyrosine kinase (BTK), a non-receptor cytoplasmic tyrosine kinase belonging to the Tec kinase family, plays a critical role in B-cell development and signaling. Discovered in 1993. BTK is named after Dr. Ogden Bruton, who first described X-linked agammaglobulinemia (XLA), a primary immunodeficiency caused by BTK gene mutations. BTK is activated downstream of the B-cell receptor (BCR) and regulates pathways involved in cell proliferation, survival, and differentiation. Dysregulated BTK signaling is implicated in B-cell malignancies (e.g., chronic lymphocytic leukemia, mantle cell lymphoma) and autoimmune disorders.
BTK inhibitors, such as ibrutinib, acalabrutinib, and zanubrutinib, have revolutionized treatment for B-cell cancers by covalently binding to BTK’s active site, blocking BCR signaling. These therapies improve survival but face challenges like off-target effects and resistance mutations. Research continues to develop next-generation inhibitors with improved selectivity and non-covalent binding mechanisms. Beyond oncology, BTK inhibitors are being explored in autoimmune diseases (e.g., rheumatoid arthritis, multiple sclerosis) due to their role in modulating immune responses. Antibodies targeting BTK are less common but may serve as research tools for studying BTK expression or signaling pathways. Overall, BTK remains a pivotal therapeutic target, bridging immunology and oncology.
×
