| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GLOD4 |
| Uniprot No | Q9HC38-2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-298aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMAARRALHFVFKVGNRFQTARFYRDVLGMK VLRHEEFEEGCKAACNGPYDGKWSKTMVGFGPEDDHFVAELTYNYGVGDY KLGNDFMGITLASSQAVSNARKLEWPLTEVAEGVFETEAPGGYKFYLQNR SLPQSDPVLKVTLAVSDLQKSLNYWCNLLGMKIYEKDEEKQRALLGYADN QCKLELQGVKGGVDHAAAFGRIAFSCPQKELPDLEDLMKRENQKILTPLV SLDTPGKATVQVVILADPDGHEICFVGDEAFRELSKMDPEGSKLLDDAMA ADKSDEWFAKHNKPKASG |
| 预测分子量 | 35 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. |
以下是假设存在的关于GLOD4重组蛋白的参考文献示例(注：实际文献可能需要通过学术数据库验证)：
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1. **标题**: "Recombinant Expression and Functional Characterization of Human GLOD4 in Bacterial Systems"
**作者**: Zhang Y, et al.
**摘要**: 研究报道了在大肠杆菌中成功表达重组人源GLOD4蛋白，并验证其酶活性，发现其参与降解毒性代谢产物甲基乙二醛，提示其在细胞解毒中的潜在作用。
2. **标题**: "GLOD4 Knockdown Exacerbates Oxidative Stress in Cardiomyocytes: Insights from Recombinant Protein Rescue Experiments"
**作者**: Tanaka K, et al.
**摘要**: 通过重组GLOD4蛋白回补实验，证明GLOD4通过调节谷胱甘肽代谢通路减轻心肌细胞氧化损伤，为心血管疾病治疗提供新靶点。
3. **标题**: "Structural Insights into GLOD4 Catalytic Mechanism via Crystallographic Analysis of Recombinant Protein"
**作者**: Müller R, et al.
**摘要**: 解析了重组GLOD4蛋白的晶体结构，揭示其底物结合位点及催化机制，为设计针对GLOD4的小分子抑制剂奠定基础。
4. **标题**: "GLOD4 Recombinant Protein Attenuates Diabetic Nephropathy in Mouse Models"
**作者**: Gupta S, et al.
**摘要**: 动物实验表明，外源性重组GLOD4蛋白可降低糖尿病肾病模型小鼠的肾脏甲基乙二醛水平，改善肾功能障碍。
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**注意**：以上为模拟示例，实际文献需通过PubMed、Web of Science等平台检索确认。若研究领域较新或GLOD4命名存在差异，建议结合具体基因名(如HGNC符号)或功能关键词扩展搜索。
GLOD4 (Glyoxalase Domain-Containing 4) is a protein encoded by the GLOD4 gene in humans, belonging to the glyoxalase enzyme family. This family is primarily involved in cellular detoxification processes, particularly the metabolism of methylglyoxal (MG), a highly reactive byproduct of glycolysis. Methylglyoxal accumulation can lead to protein glycation, DNA damage, and oxidative stress, contributing to aging and various pathologies, including diabetes, neurodegenerative diseases, and cancer. The glyoxalase system, comprising glyoxalase I (GLO1) and glyoxalase II (GLO2), converts MG into D-lactate via a glutathione-dependent pathway. While GLOD4 shares structural homology with glyoxalases, its precise enzymatic role remains less defined. Studies suggest it may function as a deglycase or regulate redox homeostasis through mechanisms distinct from classical glyoxalases.
Recombinant GLOD4 protein is produced using expression systems like Escherichia coli or mammalian cell lines, enabling biochemical and functional studies. Its recombinant form typically retains enzymatic or binding activities critical for investigating its interaction with substrates, cofactors, or inhibitors. Research on GLOD4 has gained interest due to its potential involvement in metabolic disorders and cellular stress responses. For instance, altered GLOD4 expression has been observed in cancer models, implicating it in tumor metabolism or drug resistance. Additionally, its role in mitigating dicarbonyl stress highlights therapeutic relevance for diabetic complications. Structural characterization of recombinant GLOD4. including crystallography or mutagenesis studies, aids in elucidating its catalytic mechanism and substrate specificity. Current applications span in vitro assays, drug discovery targeting dicarbonyl detoxification pathways, and biomarker development for oxidative stress-related diseases. Further exploration of GLOD4 may uncover novel therapeutic strategies for conditions linked to MG toxicity.
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