| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PDLIM2 |
| Uniprot No | Q96JY6 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-352 aa |
| 活性数据 | MALTVDVAGP APWGFRITGG RDFHTPIMVT KVAERGKAKD ADLRPGDIIV AINGESAEGM LHAEAQSKIR QSPSPLRLQL DRSQATSPGQ TNGDSSLEVL ATRFQGSVRT YTESQSSLRS SYSSPTSLSP RAGSPFSPPP SSSSLTGEAA ISRSFQSLAC SPGLPAADRL SYSGRPGSRQ AGLGRAGDSA VLVLPPSPGP RSSRPSMDSE GGSLLLDEDS EVFKMLQENR EGRAAPRQSS SFRLLQEALE AEERGGTPAF LPSSLSPQSS LPASRALATP PKLHTCEKCS TSIANQAVRI QEGRYRHPGC YTCADCGLNL KMRGHFWVGD ELYCEKHARQ RYSAPATLSS RA |
| 分子量 | 37.4 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | 0 |
| 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. |
以下是关于重组人PDLIM2蛋白的3篇文献信息(基于已有知识归纳，非真实文献)：
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1. **标题**：*PDLIM2 inhibits TGF-β-induced epithelial-mesenchymal transition of human hepatocytes by stabilizing Smad7*
**作者**：Yang L, et al.
**摘要**：研究通过重组人PDLIM2蛋白表达，发现其能与Smad7结合并抑制TGF-β信号通路，从而阻止肝细胞的上皮-间质转化(EMT)，为肝纤维化治疗提供潜在靶点。
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2. **标题**：*Structural basis of PDLIM2 in regulating NF-κB signaling through ubiquitination*
**作者**：Chen X, et al.
**摘要**：解析重组人PDLIM2蛋白的晶体结构，发现其PDZ和LIM结构域协同招募E3泛素连接酶，促进NF-κB的泛素化降解，揭示其在炎症反应中的调控机制。
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3. **标题**：*Recombinant PDLIM2 suppresses breast cancer metastasis by targeting focal adhesion dynamics*
**作者**：Wang Y, et al.
**摘要**：实验表明，重组PDLIM2蛋白通过干扰黏着斑激酶(FAK)的活性，抑制乳腺癌细胞的迁移和侵袭，提示其作为肿瘤治疗生物标志物的潜力。
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**注**：以上文献为虚拟案例，实际文献需通过PubMed、Google Scholar等平台以“PDLIM2”或“recombinant PDLIM2”为关键词检索获取。
**Background of PDLIM2 Protein**
PDLIM2 (PDZ and LIM domain protein 2), also known as mystique or SLIM, is a cytoskeletal protein encoded by the *PDLIM2* gene in humans. It belongs to the ALP (actinin-associated LIM protein) family, characterized by a unique N-terminal PDZ domain and a C-terminal LIM domain. These domains enable PDLIM2 to act as a scaffold protein, mediating protein-protein interactions critical for cellular signaling, cytoskeletal organization, and transcriptional regulation.
PDLIM2 plays a dual role in cellular processes, particularly in cancer. It can act as a tumor suppressor by targeting oncogenic transcription factors (e.g., NF-κB, STAT3) for proteasomal degradation via the ubiquitin-proteasome system, thereby inhibiting proliferation and metastasis. Conversely, in certain contexts, PDLIM2 promotes tumor progression by stabilizing β-catenin or enhancing TGF-β signaling, indicating context-dependent functionality. It also regulates cell adhesion and motility by interacting with actin-binding proteins (e.g., α-actinin), influencing epithelial-mesenchymal transition (EMT).
Beyond cancer, PDLIM2 is implicated in immune regulation, inflammation, and cardiovascular diseases. Its expression varies across tissues, with dynamic shuttling between the cytoplasm and nucleus, modulated by phosphorylation. Dysregulation of PDLIM2 is linked to pathological conditions, making it a potential therapeutic target. However, its precise mechanisms remain under investigation, highlighting the need for further research into its tissue-specific roles and signaling networks.
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