| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CRELD1 |
| Uniprot No | Q96HD1-1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-362aa |
| 氨基酸序列 | MAPWPPKGLV PAMLWGLSLF LNLPGPIWLQ PSPPPQSSPP PQPHPCHTCR GLVDSFNKGL ERTIRDNFGG GNTAWEEENL SKYKDSETRL VEVLEGVCSK SDFECHRLLE LSEELVESWW FHKQQEAPDL FQWLCSDSLK LCCPAGTFGP SCLPCPGGTE RPCGGYGQCE GEGTRGGSGH CDCQAGYGGE ACGQCGLGYF EAERNASHLV CSACFGPCAR CSGPEESNCL QCKKGWALHH LKCVDIDECG TEGANCGADQ FCVNTEGSYE CRDCAKACLG CMGAGPGRCK KCSPGYQQVG SKCLDVDECE TEVCPGENKQ CENTEGGYRC ICAEGYKQME GICVKEQIPE SAGFFSEMTE DE |
| 预测分子量 | 37 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CRELD1重组蛋白的3篇参考文献示例(注：部分为模拟文献，仅供参考格式)：
1. **标题**：*"Recombinant CRELD1 Protein Regulates Notch Signaling in Cardiac Development"*
**作者**：Smith J, et al.
**摘要**：本研究成功在大肠杆菌中表达并纯化重组CRELD1蛋白，证实其通过调控Notch信号通路影响心脏房室隔发育，为先天性心脏病机制提供新见解。
2. **标题**：*"Structural and Functional Analysis of CRELD1 Reveals Its Role in Endoplasmic Reticulum Stress Response"*
**作者**：Zhang Y, et al.
**摘要**：利用昆虫细胞系统表达重组CRELD1蛋白，结合晶体结构解析发现其通过结合内质网伴侣蛋白GRP78参与应激反应，提示其在细胞稳态中的功能。
3. **标题**：*"CRELD1 Mutations Impair Protein Secretion and Extracellular Matrix Assembly in vitro"*
**作者**：Johnson R, et al.
**摘要**：通过HEK293细胞表达野生型与突变型重组CRELD1.发现致病突变导致蛋白分泌缺陷并破坏细胞外基质形成，关联房室间隔缺损的分子机制。
(注：以上文献为示例模型，实际引用需核实真实数据库如PubMed或Google Scholar。)
CRELD1 (Cysteine-Rich with EGF-Like Domains 1) is a secreted glycoprotein implicated in cell adhesion, signaling, and developmental processes. Initially identified as a regulator of cardiac development, it plays a critical role in heart morphogenesis, particularly in atrioventricular septation. Mutations in the CRELD1 gene are associated with congenital heart defects, notably atrioventricular septal defects (AVSDs), often observed in Down syndrome patients. Beyond cardiogenesis, CRELD1 is expressed in diverse tissues, including the pancreas and nervous system, suggesting broader functional roles in cellular homeostasis and disease.
Recombinant CRELD1 protein is engineered to study its molecular mechanisms and therapeutic potential. Produced via heterologous expression systems (e.g., mammalian HEK293 or insect cells), the recombinant protein retains post-translational modifications critical for its activity. Its structure includes multiple conserved domains: an N-terminal signal peptide, two EGF-like domains involved in protein interactions, and a cysteine-rich region stabilizing conformational flexibility. These features enable CRELD1 to interact with components of the Notch signaling pathway and extracellular matrix proteins, influencing cell differentiation and tissue patterning.
Research applications of recombinant CRELD1 span in vitro assays (e.g., binding studies, cell migration assays) and in vivo models to elucidate its role in developmental disorders and cancer. Dysregulated CRELD1 expression has been linked to tumor progression, immune modulation, and fibrosis, highlighting its pathophysiological relevance. Purification often involves affinity tags (e.g., His-tag) followed by functional validation via bioactivity tests. Despite progress, its precise signaling partners and mechanistic pathways remain partially characterized, driving ongoing studies to explore CRELD1 as a biomarker or therapeutic target for congenital and acquired diseases.
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