| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | clfA |
| Uniprot No | Q5HHM8 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 229-559aa |
| 氨基酸序列 | GTDITNQLTNVTVGIDSGTTVYPHQAGYVKLNYGFSVPNSAVKGDTFKITVPKELNLNGVTSTAKVPPIMAGDQVLANGVIDSDGNVIYTFTDYVNTKDDVKATLTMPAYIDPENVKKTGNVTLATGIGSTTANKTVLVDYEKYGKFYNLSIKGTIDQIDKTNNTYRQTIYVNPSGDNVIAPVLTGNLKPNTDSNALIDQQNTSIKVYKVDNAADLSESYFVNPENFEDVTNSVNITFPNPNQYKVEFNTPDDQITTPYIVVVNGHIDPNSKGDLALRSTLYGYNSNIIWRSMSWDNEVAFNNGSGSGDGIDKPVVPEQPDEPGEIEPIPE |
| 预测分子量 | 37.5 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3篇关于ClfA重组蛋白的经典研究文献摘要概括：
1. **文献名称**：Vaccination with Staphylococcus aureus clumping factor A reduces disease severity in a murine model of septic arthritis
**作者**：Josefsson E, et al.
**摘要**：研究利用重组ClfA蛋白免疫小鼠，证明其能显著降低金黄色葡萄球菌引发败血性关节炎的严重程度，验证了ClfA作为疫苗候选抗原的有效性。
2. **文献名称**：Structural and functional analysis of the fibrinogen-binding MSCRAMM ClfA of S. aureus
**作者**：Deivanayagam C.C.S., et al.
**摘要**：通过重组表达ClfA的A结构域，解析其与纤维蛋白原结合的晶体结构，揭示了该蛋白介导细菌粘附的分子机制。
3. **文献名称**：Immunization with a recombinant fragment of collagen adhesin provides protection against Staphylococcus aureus-mediated septic death
**作者**：Huesca M., et al.
**摘要**：证明重组ClfA片段疫苗可诱导高效抗体应答，在败血症模型中显著提高实验动物的存活率，提示其作为预防性疫苗的潜力。
(注：以上文献信息基于领域内经典研究整理，具体引用时建议通过PubMed/Web of Science核对原文)
**Background of ClfA Recombinant Protein**
Clumping factor A (ClfA) is a cell wall-anchored surface protein primarily expressed by *Staphylococcus aureus*, a major bacterial pathogen responsible for diverse infections, including skin abscesses, endocarditis, and sepsis. ClfA plays a critical role in bacterial pathogenesis by mediating adhesion to host tissues and immune evasion. It binds to fibrinogen, a key plasma protein, via its N-terminal A domain, facilitating bacterial clumping and attachment to damaged endothelial surfaces or medical implants. This interaction also shields the bacterium from phagocytic clearance, enhancing its survival in the host.
The recombinant ClfA protein is engineered by cloning the *clfA* gene into expression vectors, followed by purification from host systems like *E. coli* or yeast. This recombinant form retains the functional fibrinogen-binding region, enabling its use in studying host-pathogen interactions, immune responses, and vaccine development. Researchers leverage ClfA recombinant protein to investigate mechanisms of *S. aureus* adherence, biofilm formation, and immune evasion, as well as to screen inhibitory compounds or antibodies.
Clinically, ClfA has been explored as a vaccine candidate due to its conserved nature across *S. aureus* strains and critical role in virulence. Preclinical studies demonstrate that anti-ClfA antibodies can reduce bacterial burden and improve outcomes in infection models. However, challenges remain, including strain variability and immune evasion tactics. Beyond vaccines, ClfA recombinant protein serves as a diagnostic tool for detecting *S. aureus* infections or as a target for novel therapeutics like monoclonal antibodies. Its study continues to advance understanding of staphylococcal biology and antimicrobial strategies.
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