| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DUSP22 |
| Uniprot No | Q9NRW4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-184aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMGNGMNK ILPGLYIGNF KDARDAEQLS KNKVTHILSV HDSARPMLEG VKYLCIPAAD SPSQNLTRHF KESIKFIHEC RLRGESCLVH CLAGVSRSVT LVIAYIMTVT DFGWEDALHT VRAGRSCANP NVGFQRQLQE FEKHEVHQYR QWLKEEYGES PLQDAEEAKN ILAAPGILKF WAFLRRL |
| 预测分子量 | 23 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DUSP22重组蛋白的参考文献示例(注：以下内容为模拟构造，非真实文献)：
---
1. **标题**: *"Recombinant DUSP22 Phosphatase: Expression, Purification, and Kinetic Characterization"*
**作者**: Smith A, et al.
**摘要**: 本研究报道了人源DUSP22重组蛋白在大肠杆菌中的高效表达及纯化方法，并通过体外酶活性实验证实其对MAP激酶家族成员(如JNK和p38)的特异性去磷酸化作用。研究发现DUSP22的催化效率在低底物浓度时显著高于其他DUSP成员。
2. **标题**: *"Structural Insights into DUSP22-Mediated MAP Kinase Inactivation"*
**作者**: Chen L, et al.
**摘要**: 通过X射线晶体学解析了重组DUSP22蛋白的催化结构域三维结构(分辨率2.1Å)，揭示了其独特的底物结合口袋构象。结构分析结合定点突变实验表明，DUSP22通过保守的催化基序与MAP激酶的磷酸化位点特异性结合。
3. **标题**: *"DUSP22 Recombinant Protein Suppresses T-Cell Lymphoma Proliferation via ERK Pathway Inhibition"*
**作者**: Tanaka K, et al.
**摘要**: 利用重组DUSP22蛋白处理T细胞淋巴瘤细胞系，发现其通过抑制ERK磷酸化显著降低细胞增殖和迁移能力。研究进一步证明DUSP22的缺失可导致MAPK信号通路过度激活，提示其作为肿瘤抑制因子的潜在作用。
4. **标题**: *"DUSP22 Regulates Innate Immune Response through TLR4 Signaling Modulation"*
**作者**: Wang Y, et al.
**摘要**: 通过体外重组蛋白实验和基因敲除模型，发现DUSP22直接与TLR4信号复合物相互作用，负调控NF-κB和IRF3通路的激活。研究为DUSP22在炎症性疾病中的治疗潜力提供了生化证据。
---
以上文献摘要概括了DUSP22重组蛋白在表达纯化、结构解析、肿瘤抑制及免疫调节中的关键研究，涵盖酶学特性、结构机制与病理功能。
DUSP22 (dual-specificity phosphatase 22), also known as JKAP or LMWDSP2. is a member of the protein tyrosine phosphatase (PTP) superfamily that specifically dephosphorylates both phosphotyrosine and phosphoserine/phosphothreonine residues on target proteins. It belongs to the atypical dual-specificity phosphatase (DUSP) subgroup, which regulates mitogen-activated protein kinase (MAPK) signaling pathways involved in cell proliferation, differentiation, apoptosis, and immune responses. DUSP22 primarily inactivates stress-activated MAPKs, such as JNK and p38. by removing phosphate groups, thereby modulating downstream signaling events.
Structurally, DUSP22 contains a conserved N-terminal catalytic domain responsible for phosphatase activity and a unique C-terminal region that may influence substrate specificity or subcellular localization. Unlike other DUSPs, it lacks a MAPK-binding motif, suggesting distinct regulatory mechanisms. Studies highlight its role in immune regulation, particularly in T-cell receptor signaling and NF-κB pathway modulation. Dysregulation of DUSP22 has been linked to autoimmune diseases, lymphomas, and cancers, where it may act as a tumor suppressor or oncogene depending on context. For instance, its downregulation is associated with ALK-negative anaplastic large cell lymphoma, while overexpression correlates with poor prognosis in certain solid tumors.
Recombinant DUSP22 protein is engineered using expression systems (e.g., E. coli, mammalian cells) for functional studies, enabling researchers to explore its enzymatic kinetics, substrate interactions, and therapeutic potential. Purification often involves affinity tags (e.g., His-tag) for isolation. Its recombinant form serves as a critical tool for deciphering immune signaling networks and developing targeted therapies for inflammatory disorders or cancers.
×
