| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DDIT4 |
| Uniprot No | Q9NX09 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-232aa |
| 氨基酸序列 | MPSLWDRFSS SSTSSSPSSL PRTPTPDRPP RSAWGSATRE EGFDRSTSLE SSDCESLDSS NSGFGPEEDT AYLDGVSLPD FELLSDPEDE HLCANLMQLL QESLAQARLG SRRPARLLMP SQLVSQVGKE LLRLAYSEPC GLRGALLDVC VEQGKSCHSV GQLALDPSLV PTFQLTLVLR LDSRLWPKIQ GLFSSANSPF LPGFSQSLTL STGFRVIKKK LYSSEQLLIE EC |
| 预测分子量 | 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3篇关于DDIT4重组蛋白的参考文献摘要概述：
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1. **文献名称**: *DDIT4 regulates mTOR through feedback modulation of Akt signalling*
**作者**: Kimball SR et al.
**摘要**: 研究通过大肠杆菌表达重组DDIT4蛋白，揭示其通过抑制mTORC1复合体活性参与细胞能量应激响应，证实DDIT4作为Akt/mTOR通路负反馈调节因子的分子机制。
2. **文献名称**: *Recombinant DDIT4 induces autophagy in glioblastoma cells under hypoxia*
**作者**: Wang L et al.
**摘要**: 利用HEK293细胞系统表达人源DDIT4重组蛋白，发现其在低氧条件下通过激活AMPK/ULK1通路促进胶质母细胞瘤细胞自噬，为靶向肿瘤微环境提供新策略。
3. **文献名称**: *Structural characterization of recombinant human DDIT4 by circular dichroism*
**作者**: Gupta RK et al.
**摘要**: 首次报道DDIT4重组蛋白的二级结构特征，圆二色谱分析显示其含有高比例α-螺旋，为后续研究蛋白互作及药物开发奠定结构基础。
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注：上述文献为示例性内容，实际引用需以具体论文数据为准。建议通过PubMed或Web of Science以"DDIT4 recombinant protein"为关键词检索最新研究。
**Background on DDIT4 Recombinant Protein**
DDIT4 (DNA Damage-Inducible Transcript 4), also known as REDD1 (Regulated in Development and DNA Damage Response 1) or RTP801. is a stress-responsive protein encoded by the *DDIT4* gene. It was initially identified as a hypoxia- and DNA damage-inducible molecule that plays a critical role in cellular adaptation to metabolic and environmental stressors. DDIT4 functions as a key regulator of the mTOR (mechanistic Target of Rapamycin) signaling pathway, a central hub controlling cell growth, proliferation, autophagy, and energy metabolism. Under stress conditions (e.g., hypoxia, nutrient deprivation, or DNA damage), DDIT4 is upregulated, inhibiting mTORC1 (mTOR complex 1) activity by promoting the interaction of TSC1/TSC2 complexes with Rheb, thereby suppressing cell growth and enhancing stress adaptation.
The recombinant DDIT4 protein is produced using genetic engineering techniques, typically expressed in prokaryotic (e.g., *E. coli*) or eukaryotic (e.g., mammalian or insect cell) systems, followed by purification to ensure high specificity and bioactivity. Recombinant DDIT4 serves as a valuable tool for studying mTOR pathway dynamics, cellular stress responses, and metabolic regulation. Its applications span basic research (e.g., elucidating mechanisms in cancer, diabetes, and neurodegenerative diseases) and drug discovery, particularly in targeting mTOR-related pathologies.
Dysregulation of DDIT4 has been implicated in various diseases. Overexpression is observed in certain cancers, contributing to chemoresistance and tumor survival under hypoxia. Conversely, reduced DDIT4 levels are linked to metabolic disorders, such as insulin resistance. Recombinant DDIT4 protein enables researchers to modulate mTOR activity in vitro or in vivo, aiding in the exploration of therapeutic strategies. Challenges in its use include ensuring proper post-translational modifications (critical for function) and maintaining stability during experimental workflows.
Overall, DDIT4 recombinant protein remains a pivotal reagent for dissecting stress-response pathways and developing interventions for diseases tied to mTOR signaling dysregulation.
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