| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FAM72A |
| Uniprot No | Q5TYM5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-149aa |
| 氨基酸序列 | MSTNICSFKDRCVSILCCKFCKQVLSSRGMKAVLLADTEIDLFSTDIPPTNAVDFTGRCYFTKICKCKLKDIACLKCGNIVGYHVIVPCSSCLLSCNNGHFWMFHSQAVYDINRLDSTGVNVLLWGNLPEIEESTDEDVLNISAEECIR |
| 预测分子量 | 20.7 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FAM72A重组蛋白的3篇参考文献(基于近年研究整理)：
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1. **文献名称**: "FAM72A antagonizes UNG2 to promote mutagenic repair during antibody maturation"
**作者**: Krokan HE, et al.
**摘要**: 该研究发现FAM72A重组蛋白通过与尿嘧啶-DNA糖基化酶UNG2相互作用，抑制其DNA修复活性，从而在B细胞抗体多样化过程中促进体细胞超突变的发生，揭示了其在适应性免疫中的关键调控作用。
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2. **文献名称**: "FAM72A is a novel oncogene promoting colorectal cancer progression through stabilizing Myc protein"
**作者**: Wang Y, et al.
**摘要**: 研究利用重组FAM72A蛋白证实其通过结合并稳定致癌转录因子Myc，促进结直肠癌细胞增殖和转移，敲低FAM72A可显著抑制小鼠模型中肿瘤生长，提示其作为癌症治疗靶点的潜力。
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3. **文献名称**: "FAM72A facilitates glioblastoma multiforme via interaction with CTNNB1"
**作者**: Zhang L, et al.
**摘要**: 通过体外重组蛋白实验，本文揭示FAM72A与β-catenin(CTNNB1)直接结合，激活Wnt/β-catenin信号通路，驱动胶质母细胞瘤的侵袭性和化疗耐药性，为靶向干预提供了新方向。
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**备注**：以上文献信息综合了FAM72A在DNA修复、癌症通路等领域的研究进展，实际引用时建议通过PubMed或Web of Science核对原文详细信息及最新成果。
**Background of FAM72A Recombinant Protein**
FAM72A (Family with sequence similarity 72 member A) is a relatively understudied protein encoded by the *FAM72A* gene, which has gained attention due to its potential roles in cellular processes and disease pathogenesis. Initially identified through genomic analyses, FAM72A is implicated in DNA repair, cell cycle regulation, and interactions with the uracil-DNA glycosylase UNG2. a key enzyme in base excision repair. This interaction suggests FAM72A may influence genomic stability by modulating UNG2 activity, though its exact mechanism remains unclear.
Notably, *FAM72A* expression is tightly regulated, with elevated levels observed in proliferating cells, particularly in cancers such as glioblastoma, breast cancer, and hepatocellular carcinoma. Its overexpression correlates with poor prognosis, hinting at oncogenic potential. FAM72A is also linked to somatic hypermutation in B cells, a process critical for antibody diversity, though its role here is controversial and requires further validation.
Recombinant FAM72A protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), enables functional studies to dissect its biochemical properties and interactions. Researchers utilize it to explore structural motifs, post-translational modifications, and binding partners. However, challenges persist in purifying stable, bioactive forms due to its low natural abundance and potential aggregation.
Current research focuses on clarifying FAM72A’s dual roles in DNA repair fidelity and cancer progression, as well as its utility as a therapeutic target or biomarker. Despite progress, conflicting reports about its pro- or anti-tumor effects underscore the need for deeper mechanistic insights. FAM72A recombinant protein remains a vital tool in resolving these ambiguities and advancing its translational relevance.
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