| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | C13orf12 |
| Uniprot No | Q9Y244 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-141aa |
| 氨基酸序列 | MNARGLGSELKDSIPVTELSASGPFESHDLLRKGFSCVKNELLPSHPLELSEKNFQLNQDKMNFSTLRNIQGLFAPLKLQMEFKAVQQVQRLPFLSSSNLSLDVLRGNDETIGFEDILNDPSQSEVMGEPHLMVEYKLGLL |
| 分子量 | 42.2 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. **"Characterization of C13orf12/RNF25 as a Novel Ubiquitin Ligase Involved in Stress Response"**
- **Authors**: T. Ohta, Y. Suzuki, et al.
- **Summary**: 本研究利用重组C13orf12蛋白，揭示其作为E3泛素连接酶的活性，并发现其在细胞氧化应激反应中通过泛素化修饰靶标蛋白(如HSP70)调控细胞存活。实验证明重组蛋白在体外泛素化体系中表现出酶活性。
2. **"C13orf12 Promotes Glioblastoma Progression via EGFR/STAT3 Signaling"**
- **Authors**: L. Zhang, W. Chen, et al.
- **Summary**: 通过重组C13orf12蛋白的过表达实验，研究发现其通过增强EGFR信号通路驱动胶质母细胞瘤侵袭，机制涉及STAT3磷酸化调控。重组蛋白被用于体外激酶活性分析及细胞模型验证。
3. **"C13orf12 Interacts with Mitochondrial Proteins and Modulates Apoptosis in Breast Cancer Cells"**
- **Authors**: J. Smith, R. Patel, et al.
- **Summary**: 研究利用重组C13orf12蛋白进行免疫共沉淀和蛋白质质谱分析，发现其与线粒体抗凋亡蛋白(如Bcl-2)相互作用，抑制乳腺癌细胞凋亡。重组蛋白在体外验证了蛋白互作及功能影响。
4. **"Structural Insights into C13orf12’s Role in Iron-Sulfur Cluster Biogenesis"**
- **Authors**: K. Kim, M. Tanaka, et al.
- **Summary**: 通过重组表达人源C13orf12蛋白并进行X射线晶体学分析，揭示其与铁硫簇组装复合物的结合模式，表明其在代谢酶成熟中的关键作用。结构数据支持其作为辅助因子参与线粒体能量代谢。
(注：上述文献为示例性质，实际引用需根据具体研究补充真实发表信息。)
The human C13orf12 protein, encoded by the *C13orf12* gene on chromosome 13q14.11. is a relatively understudied protein implicated in cellular transport and neurodegenerative disorders. Initially identified through genomic analyses, it spans 210 amino acids and is predicted to contain multiple transmembrane domains, suggesting a role in membrane-associated processes. Studies indicate its interaction with EAAT3 (excitatory amino acid transporter 3), modulating glutamate transport in neurons, which links it to neurotransmission and synaptic plasticity.
C13orf12 gained attention due to its association with childhood-onset neurodegenerative diseases, particularly mitochondrial complex I deficiency. Recessive mutations in *C13orf12* are linked to severe phenotypes, including hypotonia, developmental delay, and early mortality, highlighting its role in mitochondrial function. Additionally, altered expression has been observed in pediatric cancers, such as neuroblastoma, though its oncogenic mechanisms remain unclear.
Despite limited functional characterization, C13orf12 is hypothesized to act as a scaffold or regulatory protein in intracellular trafficking or redox signaling. Its conservation across vertebrates underscores potential biological significance. Ongoing research aims to clarify its molecular interactions, disease-related pathways, and therapeutic potential, particularly in mitochondrial disorders. Efforts to generate knockout models and profile tissue-specific expression patterns may further elucidate its physiological and pathological roles.
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