| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ANX1 |
| Uniprot No | P04083 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 5-346aa |
| 氨基酸序列 | SEFLKQAWFIENEEQEYVQTVKSSKGGPGSAVSPYPTFNPSSDVAALHKAIMVKGVDEATIIDILTKRNNAQRQQIKAAYLQETGKPLDETLKKALTGHLEEVVLALLKTPAQFDADELRAAMKGLGTDEDTLIEILASRTNKEIRDINRVYREELKRDLAKDITSDTSGDFRNALLSLAKGDRSEDFGVNEDLADSDARALYEAGERRKGTDVNVFNTILTTRSYPQLRRVFQKYTKYSKHDMNKVLDLELKGDIEKCLTAIVKCATSKPAFFAEKLHQAMKGVGTRHKALIRIMVSRSEIDMNDIKAFYQKMYGISLCQAILDETKGDYEKILVALCGGN |
| 预测分子量 | 42.3 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ANX1重组蛋白的3-4篇参考文献的简要概括(文献为虚拟示例，仅供参考)：
1. **文献名称**：*"Recombinant Annexin A1 Attenuates Neutrophil Migration in Sepsis via FPR2 Signaling"*
**作者**：Chen, Y. et al.
**摘要**：研究通过原核系统表达重组ANX1.发现其通过激活甲酰肽受体2(FPR2)抑制脓毒症模型中的中性粒细胞过度浸润，减轻全身炎症反应。
2. **文献名称**：*"Engineering a Stable Form of Recombinant ANX1 for Anti-inflammatory Therapy"*
**作者**：Müller, R. et al.
**摘要**：利用哺乳动物细胞系优化重组ANX1的稳定性，证明修饰后的蛋白在类风湿性关节炎模型中有效抑制促炎介质IL-6和TNF-α的释放。
3. **文献名称**：*"Recombinant ANX1 Promotes Macrophage Polarization to M2 Phenotype in Diabetic Wound Healing"*
**作者**：Wang, Q. et al.
**摘要**：研究发现重组ANX1通过调控STAT3通路，诱导巨噬细胞向M2型极化，加速糖尿病小鼠皮肤创面的愈合过程。
4. **文献名称**：*"Functional Crosstalk Between Recombinant ANX1 and Glucocorticoids in Asthma"*
**作者**：Rossi, A. et al.
**摘要**：揭示重组ANX1与糖皮质激素协同作用，增强气道上皮细胞抗炎反应，为哮喘的联合治疗提供实验依据。
注：以上文献为模拟内容，实际研究中需查阅真实数据库(如PubMed)获取准确信息。
Annexin A1 (ANX1), also known as lipocortin-1. is a member of the annexin superfamily of calcium-dependent phospholipid-binding proteins. It was first identified in the 1980s as a mediator of glucocorticoid anti-inflammatory actions. Structurally, ANX1 consists of a conserved C-terminal core domain, which facilitates interactions with phospholipid membranes in a calcium-dependent manner, and a unique N-terminal domain that regulates protein-protein interactions and cellular signaling. This protein is widely expressed in various tissues, particularly in immune cells (e.g., neutrophils, macrophages), epithelial cells, and endothelial cells.
ANX1 plays a multifaceted role in modulating inflammatory responses, apoptosis, cell proliferation, and differentiation. It is critically involved in resolving inflammation by inhibiting phospholipase A2 activity, reducing leukocyte migration, and promoting neutrophil apoptosis. Additionally, ANX1 mediates the anti-inflammatory effects of glucocorticoids, making it a key player in endogenous feedback mechanisms to control excessive inflammation. Beyond immunity, ANX1 has been implicated in cancer biology, where it exhibits context-dependent roles—either suppressing or promoting tumor progression depending on the cellular environment. It also influences cardiovascular and neurological processes, including blood vessel homeostasis and neuroprotection.
Recombinant ANX1 protein, produced via genetic engineering in systems like *E. coli* or mammalian cells, retains these functional properties and is widely used in biomedical research. It serves as a tool to study ANX1's mechanisms in inflammation-related diseases (e.g., arthritis, sepsis), cancer metastasis, and tissue repair. Therapeutic potential is being explored, including its use in anti-inflammatory therapies or as a biomarker for disease progression. Challenges remain in understanding its dual roles in different pathologies and optimizing delivery methods for clinical applications.
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