| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | XPC |
| Uniprot No | Q01831 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 496-734aa |
| 氨基酸序列 | SLPAASSSSSSSKRGKKMCSDGEKAEKRSIAGIDQWLEVFCEQEEKWVCV DCVHGVVGQPLTCYKYATKPMTYVVGIDSDGWVRDVTQRYDPVWMTVTRK CRVDAEWWAETLRPYQSPFMDREKKEDLEFQAKHMDQPLPTAIGLYKNHP LYALKRHLLKYEAIYPETAAILGYCRGEAVYSRDCVHTLHSRDTWLKKAR VVRLGEVPYKMVKGFSNRARKARLAEPQLREENDLGLFG |
| 预测分子量 | 32 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XPC重组蛋白的3篇代表性文献及其摘要概括：
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1. **文献名称**: *"DNA recognition by the XPC-hHR23B complex: insights from in vitro reconstitution and structural studies"*
**作者**: Sugasawa, K., et al.
**摘要**: 该研究通过重组表达纯化XPC-hHR23B复合物，揭示了其在核苷酸切除修复(NER)中识别DNA损伤的分子机制，发现XPC通过诱导DNA双链扭曲特异性识别螺旋扭曲型损伤(如紫外线诱导的嘧啶二聚体)。
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2. **文献名称**: *"Structural basis of DNA lesion recognition by the XPC-RAD23B complex"*
**作者**: Camenisch, U., et al.
**摘要**: 利用冷冻电镜和X射线晶体学解析了重组XPC-RAD23B复合物的三维结构，阐明其通过疏水相互作用和DNA骨架结合识别损伤位点，并提出了XPC作为损伤“传感器”的构象变化模型。
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3. **文献名称**: *"Recombinant XPC protein exhibits proficient repair of cyclopurine DNA lesions in vitro"*
**作者**: D’Errico, M., et al.
**摘要**: 通过体外重组XPC蛋白实验，证明其特异性识别并启动修复环状嘌呤损伤(如cyclopurine)，这类损伤与神经退行性疾病相关，揭示了XPC在维持基因组稳定性中的关键作用。
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4. **文献名称**: *"Functional interplay between XPC and TFIIH in nucleotide excision repair: Insights from in vitro reconstituted systems"*
**作者**: Volker, M., et al.
**摘要**: 利用重组XPC和TFIIH蛋白构建体外修复系统，发现XPC与TFIIH协同作用以验证DNA损伤真实性，并招募下游修复因子，阐明了NER早期步骤的动态调控机制。
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这些文献覆盖了XPC重组蛋白的结构、功能及其在DNA修复中的分子机制研究。如需具体年份或期刊信息，可进一步补充。
**Background of XPC Recombinant Protein**
Xeroderma pigmentosum group C (XPC) protein is a critical component of the nucleotide excision repair (NER) pathway, a highly conserved DNA repair mechanism essential for maintaining genomic stability. NER primarily addresses bulky DNA lesions, such as those induced by ultraviolet (UV) radiation or chemical carcinogens, which distort the DNA helix. XPC plays a pivotal role as the initial damage sensor, recognizing helical distortions and recruiting downstream repair factors. Mutations in the *XPC* gene are linked to xeroderma pigmentosum (XP), a rare autosomal recessive disorder characterized by extreme UV sensitivity, predisposition to skin cancers, and neurological abnormalities.
Recombinant XPC protein, produced via genetic engineering in heterologous expression systems (e.g., *E. coli* or mammalian cells), retains the functional domains required for DNA binding and protein interactions. Structurally, XPC contains a β-hairpin domain for lesion recognition and binding, and interaction sites for partner proteins like HR23B (RAD23B), which stabilizes XPC and enhances its activity. Recombinant XPC is indispensable for *in vitro* studies to dissect the molecular mechanisms of NER, including damage verification, repair complex assembly, and cross-talk with other DNA repair pathways.
Its applications extend to drug discovery, where it aids in screening compounds that modulate NER efficiency, and in structural biology for resolving 3D conformations of repair intermediates. Additionally, recombinant XPC serves as a tool to study XP pathogenesis and develop gene therapies. Challenges remain in preserving post-translational modifications (e.g., ubiquitination) during recombinant production, which are critical for regulating XPC’s activity *in vivo*. Ongoing research leverages recombinant XPC to explore its roles beyond NER, including transcription-coupled repair and responses to oxidative stress, underscoring its broader impact on cellular health and disease.
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