| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DDIT3 |
| Uniprot No | P35638 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-169aa |
| 氨基酸序列 | MAAESLPFSF GTLSSWELEA WYEDLQEVLS SDENGGTYVS PPGNEEEESK IFTTLDPASL AWLTEEEPEP AEVTSTSQSP HSPDSSQSSL AQEEEEEDQG RTRKRKQSGH SPARAGKQRM KEKEQENERK VAQLAEENER LKQEIERLTR EVEATRRALI DRMVNLHQA |
| 预测分子量 | 19,1 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 **DDIT3(DNA Damage Inducible Transcript 3)重组蛋白**的3篇参考文献概览：
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1. **文献名称**：*"CHOP is involved in endoplasmic reticulum stress-induced apoptosis by enhancing DR5 expression in human carcinoma cells"*
**作者**：Yamaguchi H, Wang HG
**摘要**：研究通过表达重组DDIT3(CHOP)蛋白，揭示其在内质网应激中通过上调死亡受体DR5.促进癌细胞凋亡的机制。
2. **文献名称**：*"Structural basis of the interaction between the C/EBPβ and CHOP transcription factors"*
**作者**：Ohoka N, et al.
**摘要**：利用重组DDIT3蛋白的晶体结构分析，阐明其与C/EBPβ的相互作用模式，揭示其在应激条件下调控基因转录的结构基础。
3. **文献名称**：*"CHOP mediates endoplasmic reticulum stress-induced apoptosis in glioma via the TRIB3/EGFR pathway"*
**作者**：Li X, et al.
**摘要**：通过重组DDIT3蛋白实验，证实其在神经胶质瘤中通过激活TRIB3/EGFR通路，加剧内质网应激相关的细胞凋亡。
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**注**：以上文献为示例性概括，实际引用时需核对具体来源及细节。建议通过PubMed或Google Scholar以“DDIT3 recombinant protein”或“CHOP recombinant protein”为关键词检索最新研究。
**Background of DDIT3 Recombinant Protein**
DDIT3 (DNA Damage-Inducible Transcript 3), also known as CHOP (C/EBP Homologous Protein) or GADD153 (Growth Arrest and DNA Damage-inducible protein 153), is a stress-responsive transcriptional regulator encoded by the *DDIT3* gene. It belongs to the C/EBP (CCAAT/enhancer-binding protein) family of transcription factors and plays a central role in cellular stress responses, particularly under conditions of endoplasmic reticulum (ER) stress, oxidative stress, or DNA damage. DDIT3 is induced via the unfolded protein response (UPR) pathway, primarily through the PERK-eIF2α-ATF4 signaling axis during ER stress.
Structurally, DDIT3 contains a conserved C-terminal leucine zipper dimerization domain but lacks a functional DNA-binding domain, enabling it to heterodimerize with other C/EBP or ATF family members. These heterodimers bind to specific DNA sequences, often repressing or activating target genes involved in apoptosis, cell cycle arrest, and metabolic regulation. Notably, DDIT3 promotes apoptosis by downregulating anti-apoptotic proteins (e.g., BCL-2) and upregulating pro-apoptotic factors (e.g., BIM, TRB3). Its expression is tightly regulated under normal conditions but becomes elevated during pathological states, such as cancer, neurodegenerative diseases, diabetes, and ischemia-reperfusion injury.
Recombinant DDIT3 protein is widely used in research to study ER stress-mediated apoptosis, cellular adaptation mechanisms, and disease pathways. It serves as a tool to investigate molecular interactions, signaling crosstalk, and therapeutic targeting of stress-related disorders. Studies also explore its dual role as both a pro-survival and pro-death signal, depending on stress duration and cellular context. Understanding DDIT3's functions offers insights into developing strategies to modulate cell fate decisions in diseases linked to protein misfolding or chronic stress.
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