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| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CREG1 |
| Uniprot No | O75629 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 32-220aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMRGGRDH GDWDEASRLP PLPPREDAAR VARFVTHVSD WGALATISTL EAVRGRPFAD VLSLSDGPPG AGSGVPYFYL SPLQLSVSNL QENPYATLTM TLAQTNFCKK HGFDPQSPLC VHIMLSGTVT KVNETEMDIA KHSLFIRHPE MKTWPSSHNW FFAKLNITNI WVLDYFGGPK IVTPEEYYNV TVQ |
| 预测分子量 | 24 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CREG1重组蛋白的3篇参考文献摘要(内容基于真实研究概括，但文献标题与作者为模拟示例)：
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1. **文献名称**: *CREG1 promotes vascular smooth muscle cell differentiation via the TGF-β signaling pathway*
**作者**: Zhang Y et al.
**摘要**: 研究通过重组CREG1蛋白体外处理平滑肌细胞，发现其通过激活TGF-β/Smad信号通路增强细胞分化，提示CREG1在血管重塑中的潜在作用。
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2. **文献名称**: *Recombinant CREG1 inhibits tumor growth by regulating lysosomal function in hepatocellular carcinoma*
**作者**: Li X et al.
**摘要**: 该研究证明重组CREG1蛋白通过促进肝癌细胞溶酶体成熟，诱导自噬依赖性细胞死亡，为靶向CREG1的肿瘤治疗提供实验依据。
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3. **文献名称**: *CREG1 recombinant protein attenuates cardiac hypertrophy through modulating ERK1/2 phosphorylation*
**作者**: Wang H et al.
**摘要**: 利用重组CREG1蛋白干预心肌肥大小鼠模型，发现其通过抑制ERK1/2过度磷酸化减轻心脏纤维化，提示其在心血管疾病中的治疗潜力。
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(注：以上文献信息为模拟，实际研究需通过数据库如PubMed检索确认。)
**Background of Recombinant CREG1 Protein**
Cellular Repressor of E1A-Stimulated Genes 1 (CREG1) is a secreted glycoprotein encoded by the *CREG1* gene in humans. Initially identified as a transcriptional repressor counteracting adenovirus E1A-mediated gene activation, CREG1 is now recognized for its broader roles in cellular homeostasis, differentiation, and tissue repair. It is ubiquitously expressed, with higher levels in organs like the heart, placenta, and kidneys. Structurally, CREG1 contains conserved N- and O-linked glycosylation sites and a functionally critical N-terminal trefoil domain, which may mediate interactions with extracellular matrix (ECM) components or cell-surface receptors.
Functionally, CREG1 regulates cell proliferation, apoptosis, and ECM remodeling. It binds to integrins or insulin-like growth factor receptors, modulating signaling pathways such as MAPK/ERK and PI3K/Akt. These interactions underpin its involvement in vascular development, angiogenesis, and tissue regeneration. Notably, CREG1 stabilizes lysosomal membranes and enhances autophagic flux, linking it to metabolic regulation and cellular stress responses.
Dysregulation of CREG1 is implicated in pathologies like cardiovascular diseases, cancer, and metabolic disorders. Reduced CREG1 levels correlate with atherosclerosis and myocardial dysfunction, while its overexpression in tumors suggests context-dependent roles in oncogenesis. Recombinant CREG1 (rCREG1), produced via bacterial or mammalian expression systems, retains bioactivity and is used to explore therapeutic potential. Preclinical studies highlight its efficacy in promoting wound healing, mitigating ischemic injury, and rescuing lysosomal storage disorders.
Despite progress, CREG1's precise mechanisms and receptor targets remain partially elusive. Ongoing research aims to clarify its role in disease and harness rCREG1 for regenerative medicine or targeted therapies.
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