| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | JAK2 |
| Uniprot No | O60674 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 513-827aa |
| 氨基酸序列 | RTNGVSDVPTSPTLQRPTHMNQMVFHKIRNEDLIFNESLGQGTFTKIFKG VRREVGDYGQLHETEVLLKVLDKAHRNYSESFFEAASMMSKLSHKHLVLN YGVCVCGDENILVQEFVKFGSLDTYLKKNKNCINILWKLEVAKQLAWAMH FLEENTLIHGNVCAKNILLIREEDRKTGNPPFIKLSDPGISITVLPKDIL QERIPWVPPECIENPKNLNLATDKWSFGTTLWEICSGGDKPLSALDSQRK LQFYEDRHQLPAPKWAELANLINNCMDYEPDFRPSFRAIIRDLNSLFTPD YELLTENDMLPNMRI |
| 预测分子量 | 39 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于JAK2重组蛋白的3篇代表性文献概览：
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1. **文献名称**：*Structural basis for JAK2 kinase activation by the V617F pathogenic mutation*
**作者**：Lupardus, P.J. 等(2014)
**摘要**：通过X射线晶体学解析了JAK2激酶结构域(JH1)的构象变化，揭示了V617F突变导致的自激活机制。该突变破坏JH1的自抑制界面，为骨髓增殖性疾病的靶向治疗提供结构依据。
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2. **文献名称**：*Activation of JAK2 catalytic activity requires phosphorylation of its activation loop tyrosine (Y1007)*
**作者**：Saharinen, P. 等(2000)
**摘要**：研究证实JAK2重组蛋白的激酶活性依赖于Y1007位点的磷酸化。通过体外重组实验证明，磷酸化后JAK2能有效激活下游STAT蛋白，阐明其信号转导的分子基础。
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3. **文献名称**：*JAK2 V617F-mediated signaling is dependent on the JAK2 kinase domain and proteasomal degradation*
**作者**：Levine, R.L. 等(2005)
**摘要**：首次在真性红细胞增多症患者中发现JAK2 V617F突变，利用重组蛋白模型证明该突变导致组成性激活，促进细胞因子非依赖性增殖，为靶向抑制剂开发奠定基础。
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4. **文献名称**：*High-throughput screening of JAK2 kinase inhibitors using a recombinant enzyme system*
**作者**：Lucet, I.S. 等(2006)
**摘要**：建立基于重组JAK2激酶结构域的高通量筛选平台，成功鉴定出ATP竞争性小分子抑制剂，为治疗骨髓增殖性肿瘤提供先导化合物。
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这些文献分别从结构生物学、信号机制、疾病关联及药物开发角度阐释了JAK2重组蛋白的关键特性。
**Background of JAK2 Recombinant Protein**
The Janus kinase 2 (JAK2) protein is a member of the JAK family of non-receptor tyrosine kinases, which play pivotal roles in cytokine and growth factor signaling. JAK2 is characterized by two tandem kinase domains: a catalytically inactive pseudokinase domain (JH2) and an active tyrosine kinase domain (JH1). It functions as a critical mediator of the JAK-STAT signaling pathway, transmitting extracellular signals from cytokines (e.g., erythropoietin, thrombopoietin) and hormones to regulate cellular processes like proliferation, differentiation, and apoptosis.
JAK2 gained significant attention due to its association with myeloproliferative neoplasms (MPNs), particularly through the somatic V617F mutation in the pseudokinase domain. This mutation constitutively activates JAK2. leading to uncontrolled hematopoietic cell growth, a hallmark of conditions like polycythemia vera and myelofibrosis. Recombinant JAK2 proteins, produced using expression systems such as *E. coli* or mammalian cells, are engineered to study its structure, function, and dysregulation. These proteins retain key domains and post-translational modifications, enabling *in vitro* analyses of kinase activity, inhibitor binding, and signaling mechanisms.
Research on recombinant JAK2 has driven the development of targeted therapies, including JAK inhibitors (e.g., ruxolitinib), which alleviate symptoms in MPN patients by suppressing hyperactive signaling. Additionally, recombinant JAK2 serves as a tool for high-throughput drug screening, structural studies (e.g., X-ray crystallography), and understanding resistance mechanisms. Its role extends to autoimmune and inflammatory diseases, where aberrant JAK-STAT signaling contributes to pathogenesis.
Overall, JAK2 recombinant protein is indispensable for deciphering its biological and pathological roles, bridging basic research with therapeutic innovation in hematologic and immune disorders.
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