| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MLKL |
| Uniprot No | Q8NB16 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-471aa |
| 氨基酸序列 | MENLKHIITLGQVIHKRCEEMKYCKKQCRRLGHRVLGLIKPLEMLQDQGK RSVPSEKLTTAMNRFKAALEEANGEIEKFSNRSNICRFLTASQDKILFKD VNRKLSDVWKELSLLLQVEQRMPVSPISQGASWAQEDQQDADEDRRAFQM LRRDNEKIEASLRRLEINMKEIKETLRQYLPPKCMQEIPQEQIKEIKKEQ LSGSPWILLRENEVSTLYKGEYHRAPVAIKVFKKLQAGSIAIVRQTFNKE IKTMKKFESPNILRIFGICIDETVTPPQFSIVMEYCELGTLRELLDREKD LTLGKRMVLVLGAARGLYRLHHSEAPELHGKIRSSNFLVTQGYQVKLAGF ELRKTQTSMSLGTTREKTDRVKSTAYLSPQELEDVFYQYDVKSEIYSFGI VLWEIATGDIPFQGCNSEKIRKLVAVKRQQEPLGEDCPSELREIIDECRA HDPSVRPSVDEILKKLSTFSK |
| 预测分子量 | 59 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MLKL重组蛋白的3篇关键文献及其摘要内容：
---
1. **文献名称**：*Mixed-lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase*
**作者**：Sun, L. et al.
**摘要**：该研究阐明了MLKL在坏死性凋亡中的核心作用，发现RIP3激酶通过磷酸化激活MLKL，导致其构象变化并形成寡聚体，最终破坏细胞膜完整性，引发细胞坏死。研究通过重组MLKL蛋白验证了其与RIP3的相互作用及磷酸化依赖的激活机制。
---
2. **文献名称**：*The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism*
**作者**：Murphy, J.M. et al.
**摘要**：本文解析了MLKL假激酶域的三维结构，揭示其在坏死性凋亡中作为分子开关的机制。通过重组MLKL蛋白的生化实验，证明RIP3介导的磷酸化诱导MLKL构象变化，使其暴露出N端螺旋束结构域，进而破坏细胞膜导致死亡。
---
3. **文献名称**：*Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis*
**作者**：Cai, Z. et al.
**摘要**：研究利用重组MLKL蛋白及突变体，证实MLKL的三聚化是其膜定位和执行坏死性凋亡的关键步骤。实验表明，MLKL的N端结构域与膜脂质结合，而C端假激酶域的自抑制状态可被RIP3磷酸化解除，从而驱动细胞死亡。
---
这些文献涵盖了MLKL的结构解析、激活机制及其在坏死性凋亡中的功能，均通过重组蛋白技术验证关键假设。
**Background of MLKL Recombinant Protein**
Mixed Lineage Kinase Domain-Like (MLKL) is a key effector protein in necroptosis, a form of regulated cell death triggered by inflammatory or stress signals. Unlike apoptosis, necroptosis involves membrane rupture and release of cellular contents, contributing to immune activation and disease pathologies. MLKL is structurally characterized by an N-terminal four-helix bundle (4HB) domain and a C-terminal pseudokinase domain. While lacking catalytic kinase activity, the pseudokinase domain regulates MLKL’s activation through phosphorylation by Receptor-Interacting Protein Kinase 3 (RIPK3) in the necrosome complex.
Upon activation, MLKL undergoes oligomerization and translocates to cellular membranes, where its 4HB domain disrupts membrane integrity, leading to cell death. Recombinant MLKL proteins, produced via expression systems like *E. coli* or mammalian cells, are essential tools for studying necroptosis mechanisms. These proteins retain structural and functional features, enabling *in vitro* analyses of phosphorylation, conformational changes, and interactions with RIPK3 or inhibitors.
Research using MLKL recombinant proteins has advanced understanding of necroptosis signaling in diseases such as ischemia-reperfusion injury, neurodegenerative disorders, and cancer. Structural studies (e.g., X-ray crystallography, cryo-EM) reveal dynamic transitions of MLKL during activation, guiding therapeutic strategies to modulate necroptosis. Inhibitors targeting MLKL’s pseudokinase or 4HB domains are under exploration to treat inflammation-driven conditions.
Overall, MLKL recombinant proteins serve as critical reagents for dissecting necroptotic pathways and developing targeted therapies, bridging molecular insights to potential clinical applications.
×
