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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CT1 |
| Uniprot No | Q16619 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2-201aa |
| 氨基酸序列 | SRREGSLEDPQTDSSVSLLPHLEAKIRQTHSLAHLLTKYAEQLLQEYVQL QGDPFGLPSFSPPRLPVAGLSAPAPSHAGLPVHERLRLDAAALAALPPLL DAVCRRQAELNPRAPRLLRRLEDAARQARALGAAVEALLAALGAANRGPR AEPPAATASAASATGVFPAKVLGLRVCGLYREWLSRTEGDLGQLLPGGSA |
| 预测分子量 | 21 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CT1(Cardiotrophin-1)重组蛋白的模拟参考文献示例，基于领域内典型研究方向整理：
1. **"Cardiotrophin-1: A novel cytokine that activates cardiac myocyte hypertrophy"**
- **作者**: Pennica, D., et al.
- **摘要**: 该研究首次克隆并表征了CT1蛋白，证明其通过激活MAPK信号通路诱导心肌细胞肥大，提示其在心脏发育和病理重塑中的作用(发表于1995年，奠基性研究)。
2. **"Signaling complexes of the CT1 receptor: Role of gp130 and LIFR"**
- **作者**: Robledo, O., et al.
- **摘要**: 揭示了CT1与受体复合物(LIFR/gp130)的结合机制，阐明其下游JAK-STAT信号通路的激活，为靶向治疗提供依据(受体机制研究，约1990年代末)。
3. **"CT1 recombinant protein attenuates myocardial ischemia-reperfusion injury via PI3K/Akt pathway"**
- **作者**: Ishikawa, M., et al.
- **摘要**: 发现重组CT1蛋白通过抑制心肌细胞凋亡和氧化应激减轻缺血再灌注损伤，突出其心脏保护潜力(实验模型研究，约2000年代初)。
4. **"Therapeutic potential of CT1 in heart failure: Preclinical evidence"**
- **作者**: Latchman, N., et al.
- **摘要**: 动物模型研究表明，重组CT1可改善心功能并延缓心力衰竭进展，支持其作为治疗靶点的转化价值(临床前研究，约2010年后)。
*注：以上为模拟示例，实际文献需通过数据库(如PubMed)检索确认。建议结合具体研究主题补充关键词(如疾病模型、信号通路)筛选文献。*
CT1 (Cardiotrophin-1) recombinant protein is a biologically active cytokine belonging to the interleukin-6 (IL-6) family, first identified in 1995 for its ability to induce cardiac myocyte hypertrophy. Structurally, CT1 shares homology with other IL-6 family members, featuring a four-helix bundle topology stabilized by disulfide bonds. It signals through a receptor complex involving glycoprotein 130 (gp130) and leukemia inhibitory factor receptor β (LIFRβ), activating downstream pathways such as JAK/STAT, MAPK, and PI3K/Akt.
Originally studied for its role in cardiovascular biology, CT1 demonstrates pleiotropic effects, including promoting cardiomyocyte survival, angiogenesis, and anti-apoptotic activity. Beyond cardiac tissue, it influences neural development, liver regeneration, and metabolic regulation. Research highlights its neuroprotective potential in models of neurodegeneration and its capacity to mitigate ischemia-reperfusion injury.
In disease contexts, CT1 is implicated in pathological hypertrophy, fibrosis, and inflammatory conditions. Paradoxically, while elevated CT1 levels correlate with adverse cardiac remodeling, exogenous administration in preclinical studies shows therapeutic promise for heart failure and tissue repair. Its recombinant form, produced via bacterial or mammalian expression systems, retains native bioactivity and is widely used in mechanistic studies and therapeutic exploration.
Recent advances focus on optimizing CT1's pharmacokinetics and tissue specificity to address challenges like short half-life and off-target effects. As a research tool, CT1 recombinant protein continues to elucidate cellular stress responses and interorgan crosstalk, positioning it as a versatile candidate for regenerative medicine and disease modulation.
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