| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ALKBH7 |
| Uniprot No | Q9BT30 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-221aa |
| 氨基酸序列 | MAGTGLLALRTLPGPSWVRGSGPSVLSRLQDAAVVRPGFLSTAEEETLSRELEPELRRRRYEYDHWDAAIHGFRETEKSRWSEASRAILQRVQAAAFGPGQTLLSSVHVLDLEARGYIKPHVDSIKFCGATIAGLSLLSPSVMRLVHTQEPGEWLELLLEPGSLYILRGSARYDFSHEILRDEESFFGERRIPRGRRISVICRSLPEGMGPGESGQPPPAC |
| 分子量 | 50.9 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 冻干粉 |
| 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. |
1. **"ALKBH7 mediates necrosis via lipid peroxidation in mitochondria"**
- **作者**: Zheng et al., 2020
- **摘要**: 研究表明ALKBH7通过调控线粒体脂质过氧化介导细胞坏死，抑制其表达可减少缺血再灌注损伤中的细胞死亡，提示其在代谢应激中的关键作用。
2. **"Alkbh7 knockout mice exhibit resistance to high-fat diet-induced obesity"**
- **作者**: Fu et al., 2017
- **摘要**: 发现ALKBH7缺失小鼠对高脂饮食诱导的肥胖和胰岛素抵抗具有抗性，其机制可能与增强线粒体脂肪酸氧化和能量代谢相关。
3. **"ALKBH7 interacts with cardiolipin to sustain mitochondrial dynamics"**
- **作者**: Liu et al., 2021
- **摘要**: 揭示ALKBH7通过结合心磷脂调控线粒体膜结构，影响线粒体分裂-融合平衡，缺失导致线粒体功能紊乱和神经元退行性表型。
4. **"ALKBH7 is a tricarboxylic acid cycle enzyme regulating citrate levels"**
- **作者**: Chen et al., 2022
- **摘要**: 提出ALKBH7通过代谢α-酮戊二酸间接调控三羧酸循环中的柠檬酸合成，影响肿瘤细胞增殖，可能成为癌症治疗的靶点。
(注：以上信息为示例性内容，实际文献需通过PubMed/Google Scholar检索核实。)
ALKBH7 is a member of the AlkB family of iron- and α-ketoglutarate-dependent dioxygenases, which are evolutionarily conserved enzymes known for their roles in nucleic acid repair and epigenetic regulation. Initially identified in humans through homology to the bacterial AlkB protein, ALKBH7 localizes primarily to mitochondria, distinguishing it from other AlkB homologs that often operate in nuclear or cytoplasmic compartments. While its exact substrate specificity remains debated, studies suggest it may process alkylation damage in mitochondrial DNA or RNA, potentially safeguarding mitochondrial genome integrity. Structurally, ALKBH7 retains the characteristic catalytic triad (His-X-Asp/Glu-Xn-His) and Fe²⁺/α-KG binding residues critical for oxidative demethylation or hydroxylation reactions.
Emerging evidence links ALKBH7 to metabolic regulation and disease pathways. It appears critical in controlling cellular apoptosis through mechanisms involving metabolite signaling, particularly in response to alkylating agents or oxidative stress. Interestingly, ALKBH7 knockout models show resistance to mitochondrial-mediated cell death, hinting at its role in stress response pathways. Clinical associations have been observed in cancer, where ALKBH7 expression levels correlate with tumor progression and chemoresistance, though its precise oncogenic or tumor-suppressive functions remain context-dependent. Current research focuses on deciphering its biochemical targets and exploring therapeutic potential in mitochondrial disorders, cancer, and metabolic syndromes. (Word count: 235)
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