| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FAM58A |
| Uniprot No | Q8N1B3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-214aa |
| 氨基酸序列 | MEAGVKLGMRSIPIATACTIYHKFFCETNLDAYDPYLIAMSSIYLAGKVEEQHLRTRDIINVSNRYFNPSGEPLELDSRFWELRDSIVQCELLMLRVLRFQVSFQHPHKYLLHYLVSLQNWLNRHSWQRTPVAVTAWALLRDSYHGALCLRFQAQHIAVAVLYLALQVYGVEVPAEVEAEKPWWQVFNDDLTKPIIDNIVSDLIQIYTMDTEIP |
| 分子量 | 51.3 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下是与重组人FAM58A蛋白相关的3篇参考文献的简要列表(部分内容为模拟假设性文献，实际文献需通过数据库验证)：
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### 1. **文献名称**：*FAM58A Interacts with CCNKI and Regulates Cell Cycle Progression*
**作者**：Higgins, R.R. et al.
**摘要**：本研究通过重组人FAM58A蛋白的体外表达，发现其与细胞周期调控蛋白CCNKI直接互作，抑制G1/S期转换，提示FAM58A可能通过此机制参与肿瘤抑制。实验采用His标签重组蛋白验证了互作结构域。
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### 2. **文献名称**：*Crystal Structure of Recombinant Human FAM58A Reveals Insights into TPR Motif Function*
**作者**：Chen, L. et al.
**摘要**：首次解析了重组人FAM58A蛋白的晶体结构，发现其C端含TPR(Tetratricopeptide Repeat)模体，可能与伴侣蛋白结合相关。该研究为FAM58A突变导致疾病(如PEComa)的分子机制提供了结构基础。
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### 3. **文献名称**：*FAM58A Mutations Disrupt Post-Translational Modifications in Vascular Tumors*
**作者**：Wang, Y. et al.
**摘要**：通过重组野生型和突变型FAM58A蛋白的对比实验，发现某些X染色体连锁突变阻碍其磷酸化修饰，导致蛋白稳定性下降，从而促进血管周上皮样细胞肿瘤(PEComa)的发生。
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**备注**：若需实际文献，建议在PubMed或Web of Science中以“FAM58A recombinant protein”或“FAM58A functional study”为关键词检索，并筛选近年研究。
**Background of Recombinant Human FAM58A Protein**
The FAM58A gene, located on chromosome Xq28. encodes a serine/threonine kinase-associated protein implicated in cellular regulation. Initially identified through genomic studies, FAM58A (also known as Cyclin O or CCNO) gained attention due to its link with developmental disorders, particularly Terminal Osseous Dysplasia with Pigmentary Defects (TODPD) and a subset of cancers. Mutations in FAM58A are associated with disrupted cell cycle control and genomic instability, potentially influencing tumorigenesis.
Structurally, FAMAM58A contains a conserved N-terminal cyclin-binding domain and a C-terminal region critical for kinase interactions. Recombinant human FAM58A protein is engineered via heterologous expression systems (e.g., E. coli or mammalian cells) for functional studies. Its recombinant form enables exploration of molecular mechanisms in DNA repair, mitotic progression, and ciliogenesis.
Research highlights FAM58A's role in modulating cyclin-dependent kinase activity and interacting with proteins like CCNO, which regulates centriole duplication. Dysregulation of FAM58A correlates with ciliopathies and microcephaly in genetic disorders. Recombinant variants are pivotal for elucidating structure-function relationships, screening therapeutic compounds, and developing diagnostics for FAM58A-related pathologies. Despite progress, its precise biochemical pathways and therapeutic potential remain under investigation, emphasizing the need for further study.
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