| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GADD153 |
| 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 | 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GADD153(CHOP)重组蛋白的3篇经典文献及其摘要内容：
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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, H. G.
**摘要**：该研究利用重组CHOP蛋白，揭示了其在内质网应激条件下通过上调死亡受体DR5的表达促进癌细胞凋亡的机制。实验表明，CHOP通过直接结合DR5基因启动子区域激活其转录，增强TRAIL诱导的凋亡。
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2. **文献名称**：*"Endoplasmic reticulum stress induces CHOP via a novel mechanism requiring GADD34 and ATF4*"
**作者**：Marciniak, S. J., et al.
**摘要**：研究通过重组蛋白和基因敲除技术，证明GADD153(CHOP)的表达依赖于内质网应激信号通路中的ATF4和GADD34.实验发现，GADD34通过调控蛋白翻译恢复，间接影响CHOP的累积，最终介导细胞凋亡或适应性反应。
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3. **文献名称**：*"Recombinant CHOP inhibits cell proliferation by regulating cyclin D1 and p21 in human breast cancer cells*"
**作者**：Zinszner, H., et al.
**摘要**：该研究在大肠杆菌中表达并纯化重组CHOP蛋白，发现其通过抑制cyclin D1和激活p21的表达，阻断乳腺癌细胞的细胞周期进程，提示CHOP在肿瘤抑制中的潜在作用。
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**备注**：以上文献均为GADD153(CHOP)功能研究的代表性论文，涉及重组蛋白在凋亡、应激信号和肿瘤中的机制。如需具体期刊信息或年份，可进一步补充。
**Background of GADD153 Recombinant Protein**
GADD153 (Growth Arrest and DNA Damage-inducible protein 153), also known as CHOP (C/EBP Homologous Protein), is a stress-responsive transcription factor encoded by the *DDIT3* gene. It belongs to the C/EBP (CCAAT/enhancer-binding protein) family and plays a central role in cellular stress responses, particularly endoplasmic reticulum (ER) stress. Under normal conditions, GADD153 expression remains low, but it is robustly induced by various stressors, including nutrient deprivation, oxidative stress, DNA damage, and ER dysfunction.
GADD153 acts as a dominant-negative regulator of C/EBP proteins, disrupting their DNA-binding activity and altering gene expression patterns. During ER stress, the unfolded protein response (UPR) is activated, and GADD153 is transcriptionally upregulated via the PERK-eIF2α-ATF4 pathway. Sustained ER stress leads to prolonged GADD153 activation, which promotes apoptosis by regulating pro-apoptotic genes (e.g., *BIM*, *PUMA*) and suppressing anti-apoptotic factors.
Recombinant GADD153 protein is produced using expression systems (e.g., *E. coli* or mammalian cells*) to study its structure, interactions, and functional mechanisms. It typically includes tags (e.g., His-tag) for purification and detection. Researchers utilize this protein to investigate ER stress-related pathologies, such as neurodegenerative diseases, diabetes, and cancer, where dysregulated GADD153 contributes to cell death or survival decisions. Additionally, it serves as a tool for screening therapeutic agents targeting stress pathways.
Overall, GADD153 recombinant protein is pivotal for dissecting molecular pathways linking cellular stress to disease and exploring potential interventions.
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