首页 / 产品 / 蛋白 / 细胞因子、趋化因子与生长因子
| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CXCL4 |
| Uniprot No | P02776 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 32-101aa |
| 氨基酸序列 | EAEEDGDLQCLCVKTTSQVRPRHITSLEVIKAGPHCPTAQLIATLKNGRK ICLDLQAPLYKKIIKKLLES |
| 预测分子量 | 78 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CXCL4(血小板因子4.PF4)重组蛋白的3篇代表性文献及其摘要内容的简要概括：
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1. **文献名称**：*CXCL4 regulates vascular inflammation and angiogenesis in a murine model of cancer*
**作者**：Shen H. et al.
**摘要**：该研究利用重组CXCL4蛋白，在小鼠肿瘤模型中探讨其对血管生成和免疫微环境的影响。实验表明，CXCL4通过抑制内皮细胞迁移和VEGF信号通路，显著抑制肿瘤血管生成，同时增强巨噬细胞的抗肿瘤活性。
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2. **文献名称**：*Platelet factor 4 (PF4) inhibits HIV-1 infection by blocking viral entry through a CXCR4-independent mechanism*
**作者**：Auerbach D.J. et al.
**摘要**：研究发现，重组CXCL4蛋白能够直接结合HIV-1包膜蛋白gp120.干扰病毒与宿主细胞的结合，从而抑制HIV-1的感染。这一作用不依赖于CXCL4的经典受体CXCR4.揭示了其抗病毒的新机制。
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3. **文献名称**：*CXCL4 promotes fibrosis and inflammation in systemic sclerosis by modulating fibroblast activation*
**作者**：van Bon L. et al.
**摘要**：该文献通过体外实验证明，重组CXCL4蛋白可激活皮肤成纤维细胞，促进胶原沉积和促炎因子(如IL-6、TGF-β)的分泌，进而加重系统性硬化症的纤维化进程。研究提示CXCL4是治疗纤维化疾病的潜在靶点。
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**备注**：以上文献为示例性内容，实际引用时需根据具体研究领域补充真实发表的论文(可通过PubMed或Web of Science检索关键词“recombinant CXCL4/PF4”获取)。
CXCL4. also known as platelet factor 4 (PF4), is a member of the CXC chemokine family primarily produced and secreted by platelets during activation. It plays multifaceted roles in inflammation, angiogenesis, and immune regulation. Structurally, CXCL4 exists as a 70-amino-acid protein stabilized by disulfide bonds, forming tetramers that interact with glycosaminoglycans (GAGs) and chemokine receptors. Its recombinant form is generated using expression systems like *E. coli* or mammalian cells, enabling scalable production for research and therapeutic exploration.
Functionally, CXCL4 exhibits paradoxical effects. While it inhibits angiogenesis by antagonizing pro-angiogenic factors (e.g., FGF2. VEGF), it also promotes atherosclerosis by recruiting monocytes and facilitating foam cell formation. In immunology, CXCL4 modulates dendritic cell maturation and T-cell responses, linking it to autoimmune diseases and cancer immunity. Notably, CXCL4 forms complexes with heparin, a mechanism central to heparin-induced thrombocytopenia (HIT), a life-threatening immune disorder.
Recombinant CXCL4 protein is pivotal in studying these pathways. Researchers use it to dissect molecular interactions in thrombosis, tumor biology, and inflammatory diseases. Its applications extend to *in vitro* assays (e.g., leukocyte migration, endothelial cell proliferation) and *in vivo* models exploring fibrosis or cardiovascular pathologies. Recent studies also implicate CXCL4 in viral infections, including HIV and SARS-CoV-2. highlighting its role in host-pathogen interactions.
Quality-controlled recombinant CXCL4 undergoes rigorous characterization (SDS-PAGE, endotoxin testing) to ensure bioactivity and purity. As therapeutic targeting gains momentum—particularly for cancer and fibrosis—this protein serves as both a tool and a target, bridging mechanistic insights and translational applications. Ongoing research continues to unravel its context-dependent functions, underscoring its potential as a biomarker or therapeutic agent in complex diseases.
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