| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GPX4 |
| Uniprot No | P36969 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 29-197aa |
| 氨基酸序列 | CASRDDWRCARSMHEFSAKDIDGHMVNLDKYRGFVCIVTNVASQSGKTEVNYTQLVDLHARYAECGLRILAFPCNQFGKQEPGSNEEIKEFAAGYNVKFDMFSKICVNGDDAHPLWKWMKIQPKGKGILGNAIKWNFTKFLIDKNGCVVKRYGPMEEPLVIEKDLPHYF |
| 预测分子量 | 21.4 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GPX4重组蛋白的3篇代表性文献及摘要概括：
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1. **文献名称**: *Glutathione peroxidase 4 senses and translates oxidative stress into 12/15-lipoxygenase dependent- and AIF-mediated cell death*
**作者**: Seiler, A. et al.
**摘要**: 该研究揭示了GPX4通过抑制脂质过氧化调控细胞死亡的机制。通过重组GPX4蛋白实验，发现其缺失会导致12/15-脂氧合酶途径激活，进而引发铁死亡和凋亡诱导因子(AIF)介导的细胞死亡，提示GPX4在抗氧化防御中的核心作用。
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2. **文献名称**: *Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis*
**作者**: Ingold, K. et al.
**摘要**: 研究通过重组GPX4蛋白及突变体分析，证实硒元素在GPX4酶活性中的必要性。结果表明，硒依赖的GPX4通过清除脂质过氧化物抑制铁死亡，而硒缺失或GPX4失活会直接导致细胞铁死亡，为抗氧化治疗提供了理论依据。
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3. **文献名称**: *Structural basis for the catalytic activity of human glutathione peroxidase 4*
**作者**: Scheerer, P. et al.
**摘要**: 通过重组人源GPX4蛋白的晶体结构解析，阐明了其催化活性中心的构象及底物结合机制。研究发现GPX4通过独特的硫氧还蛋白结合域调控脂质过氧化物还原，为设计靶向GPX4的小分子药物提供了结构基础。
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4. **文献名称**: *GPX4 regulates tumor cell proliferation via modulating ferroptosis sensitivity*
**作者**: Yang, W.S. et al.
**摘要**: 利用重组GPX4蛋白及基因编辑技术，证明GPX4在癌细胞中通过抑制铁死亡促进肿瘤生长。抑制GPX4活性可增强癌细胞的铁死亡敏感性，提示其作为癌症治疗靶点的潜力。
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这些研究从分子机制、结构生物学及疾病关联等角度解析了GPX4重组蛋白的功能与应用价值。
**Background of GPX4 Recombinant Protein**
Glutathione peroxidase 4 (GPX4), a member of the glutathione peroxidase family, is a critical selenoprotein that protects cells from oxidative damage by reducing lipid hydroperoxides to nontoxic alcohols. Unlike other GPX isoforms, GPX4 uniquely targets complex membrane-bound lipid peroxides, making it indispensable for maintaining redox homeostasis and preventing ferroptosis—a form of iron-dependent, oxidative cell death. Its activity relies on glutathione (GSH) as a cofactor and incorporates selenocysteine at its catalytic site, which is encoded by a UGA stop codon recoded via a selenocysteine insertion sequence (SECIS).
GPX4 exists in three isoforms (cytosolic, mitochondrial, and nuclear) due to alternative translation initiation, enabling compartment-specific antioxidant roles. Structurally, recombinant GPX4 is typically produced in expression systems (e.g., *E. coli* or mammalian cells*) to study its enzymatic mechanisms or therapeutic potential. Recombinant forms retain the ability to inhibit lipid peroxidation and ferroptosis, making them valuable tools for exploring diseases linked to oxidative stress, such as neurodegeneration, ischemia-reperfusion injury, and cancer.
In cancer biology, GPX4 is a key survival factor for tumor cells, particularly those resistant to conventional therapies. Pharmacological inhibition of GPX4 triggers ferroptosis, a strategy under investigation for targeting therapy-resistant cancers. Conversely, GPX4 supplementation has shown protective effects in models of neurodegenerative disorders like Alzheimer’s and Parkinson’s diseases.
Challenges in producing functional recombinant GPX4 include ensuring proper selenocysteine incorporation and protein stability. Advances in expression systems and codon optimization have improved yields, enabling broader research and therapeutic exploration. Overall, GPX4 recombinant protein serves as a pivotal reagent for dissecting redox biology and developing interventions against oxidative stress-related pathologies.
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