| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SDHAF2 |
| Uniprot No | Q9NX18 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 30-166aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSSFRRFYR GDSPTDSQKD MIEIPLPPWQ ERTDESIETK RARLLYESRK RGMLENCILL SLFAKEHLQH MTEKQLNLYD RLINEPSNDW DIYYWATEAK PAPEIFENEV MALLRDFAKN KNKEQRLRAP DLEYLFEKPR |
| 预测分子量 | 19 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SDHAF2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**: *SDHAF2 mutations are associated with hereditary paraganglioma*
**作者**: Hao, H. X., et al. (2009)
**摘要**: 该研究首次克隆并表达了人源SDHAF2重组蛋白，发现其突变导致线粒体复合体II(琥珀酸脱氢酶)功能缺陷，揭示了SDHAF2在副神经节瘤遗传易感性中的作用机制。
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2. **文献名称**: *SDHAF2 (PGL2-SDH5) deficiency causes a mitochondrial complex II defect*
**作者**: Ghezzi, D., et al. (2009)
**摘要**: 通过重组蛋白表达和酵母互补实验，证明SDHAF2是复合体II组装的关键因子，其缺失导致复合体II酶活性丧失，并阐明了相关致病突变的分子基础。
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3. **文献名称**: *Epigenetic silencing of SDHAF2 in colorectal cancer*
**作者**: Bayley, J. P., et al. (2010)
**摘要**: 研究利用重组SDHAF2蛋白进行功能验证，发现结直肠癌中SDHAF2启动子甲基化导致其表达沉默，并证实其通过调控复合体II功能影响肿瘤代谢重编程。
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**备注**：上述文献为SDHAF2功能研究的早期经典论文，侧重重组蛋白在分子机制探索中的应用。近年研究可能涉及更精细的结构或治疗应用(如2020年后文献)，建议通过PubMed/Google Scholar以“SDHAF2 recombinant”为关键词获取最新进展。
SDHAF2 (Succinate Dehydrogenase Complex Assembly Factor 2) is a nuclear-encoded protein critical for the assembly and function of mitochondrial complex II (succinate dehydrogenase, SDH), a key enzyme in both the tricarboxylic acid (TCA) cycle and the electron transport chain. SDHAF2 facilitates the insertion of flavin adenine dinucleotide (FAD) cofactors into the SDHA subunit, ensuring proper enzymatic activity. Dysfunction in SDHAF2 disrupts SDH assembly, leading to metabolic and respiratory deficiencies linked to tumorigenesis, particularly in hereditary paragangliomas and pheochromocytomas.
Recombinant SDHAF2 protein is produced via heterologous expression systems (e.g., E. coli, mammalian cells) using genetic engineering techniques. This allows large-scale production of the protein for functional studies, structural analysis, and therapeutic exploration. Researchers utilize recombinant SDHAF2 to investigate its role in SDH biogenesis, characterize pathogenic mutations (e.g., germline variants like p.Gly78Arg), and model mitochondrial disorders. Its applications extend to studying metabolic reprogramming in cancers, where SDH deficiency alters succinate levels, influencing hypoxia-inducible factor (HIF) signaling and promoting tumor growth.
The protein’s conserved structure, including its LYR motif (a signature of proteins involved in iron-sulfur cluster biogenesis), makes it a focus for understanding mitochondrial complex assembly mechanisms. Recombinant SDHAF2 also serves as a tool for developing targeted therapies, such as stabilizing SDH in mutation-associated cancers or correcting assembly defects. Studies using this protein have advanced insights into how mitochondrial dysfunction contributes to rare genetic syndromes and broader metabolic diseases, bridging gaps between basic biochemistry and clinical oncology.
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