| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ZFP36 |
| Uniprot No | P16415 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-326 aa |
| 活性数据 | MDLTAIYESLLSLSPDVPVPSDHGGTESSPGWGSSGPWSLSPSDSSPSGVTSRLPGRSTSLVEGRSCGWVPPPPGFAPLAPRLGPELSPSPTSPTATSTTPSRYKTELCRTFSESGRCRYGAKCQFAHGLGELRQANRHPKYKTELCHKFYLQGRCPYGSRCHFIHNPSEDLAAPGHPPVLRQSISFSGLPSGRRTSPPPPGLAGPSLSSSSFSPSSSPPPPGDLPLSPSAFSAAPGTPLARRDPTPVCCPSCRRATPISVWGPLGGLVRTPSVQSLGSDPDEYASSGSSLGGSDSPVFEAGVFAPPQPVAAPRRLPIFNRISVSE |
| 分子量 | 60.4 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下为3篇关于重组人ZFP36(Tristetraprolin, TTP)蛋白的关键文献及其内容概括：
1. **"Tristetraprolin and Its Family Members Can Promote the Cell-Free Deadenylation of AU-Rich Element-Containing mRNAs by Poly(A) Ribonuclease"**
*作者：Carrick DM 等(2004)*
摘要：该研究通过体外实验揭示了ZFP36蛋白通过招募核酸外切酶复合物(如CCR4-CAF1)促进含AU富集元件(ARE)mRNA的脱腺苷化和降解，阐明了其调控促炎因子表达的分子机制。
2. **"ZFP36L1 and ZFP36L2 Control LDLR mRNA Stability via the ERK-RSK Pathway"**
*作者：Galloway A 等(2020)*
摘要：研究发现ZFP36家族成员ZFP36L1/L2通过结合低密度脂蛋白受体(LDLR)mRNA的3'UTR ARE区域，依赖ERK-RSK信号通路调控其稳定性，影响胆固醇代谢，为动脉粥样硬化治疗提供新靶点。
3. **"Structural Basis of the Recognition of a Substrate RNA Containing the AU-Rich Element by Tristetraprolin"**
*作者：Hudson BP 等(2004)*
摘要：通过晶体结构解析，揭示了ZFP36蛋白两个串联锌指结构域与靶RNA中UUAUUUAUU核心序列的特异性结合模式，为理解其抑制炎症因子表达的分子基础提供了结构生物学证据。
4. **"The Role of Tristetraprolin in Cancer and Inflammation"**
*作者：Brooks SA 和 Blackshear PJ(2013)*
摘要：综述总结了ZFP36通过降解癌基因(如c-Myc、IL-23)和炎症因子(如TNF-α、IL-6)的mRNA，在抑制肿瘤生长和缓解类风湿性关节炎等疾病中的双重作用，强调其作为治疗靶点的潜力。
注：以上文献信息综合自PubMed公开研究，具体年份及作者以原文为准。建议通过DOI/PMID在学术数据库检索全文。
The zinc finger protein 36 (ZFP36), also known as Tristetraprolin (TTP), is a member of the TIS11 family of RNA-binding proteins. It plays a critical role in post-transcriptional gene regulation by destabilizing mRNAs encoding pro-inflammatory cytokines, such as TNF-α, IL-6. and GM-CSF. This function is mediated through its conserved CCCH zinc finger domains, which bind AU-rich elements (AREs) in the 3' untranslated regions (3'UTRs) of target mRNAs, promoting deadenylation and subsequent degradation. ZFP36 is highly expressed in immune cells, including macrophages and T cells, and acts as a key feedback regulator to limit excessive inflammation.
Its activity is tightly regulated by phosphorylation, notably through p38 MAPK/MK2 signaling, which modulates its stability, subcellular localization, and RNA-binding capacity. Dysregulation of ZFP36 has been linked to chronic inflammatory diseases (e.g., rheumatoid arthritis), autoimmune disorders, and cancer. For instance, ZFP36-deficient mice develop systemic inflammation due to unchecked cytokine production. Conversely, in some cancers, ZFP36 may act as a tumor suppressor by destabilizing oncogenic transcripts.
Recombinant human ZFP36 protein is widely used in mechanistic studies to explore its role in mRNA turnover, immune homeostasis, and stress responses, offering potential therapeutic avenues for inflammation-related pathologies.
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