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Recombinant Human C1QTNF9 protein

  • 中文名: C1q肿瘤坏死因子相关蛋白9(C1QTNF9)重组蛋白
  • 别    名: C1QTNF9;C1QTNF9A;Complement C1q and tumor necrosis factor-related protein 9A
货号: PA1000-7763
Price: ¥询价
数量:
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产品详情

纯度>85%SDS-PAGE.
种属Human
靶点C1QTNF9
Uniprot No P0C862
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间20-333aa
氨基酸序列Q DTCRQGHPGI PGNPGHNGLP GRDGRDGAKG DKGDAGEPGR PGSPGKDGTS GEKGERGADG KVEAKGIKGD QGSRGSPGKH GPKGLAGPMG EKGLRGETGP QGQKGNKGDV GPTGPEGPRG NIGPLGPTGL PGPMGPIGKP GPKGEAGPTG PQGEPGVRGI RGWKGDRGEK GKIGETLVLP KSAFTVGLTV LSKFPSSDMP IKFDKILYNE FNHYDTAAGK FTCHIAGVYY FTYHITVFSR NVQVSLVKNG VKILHTKDAY MSSEDQASGG IVLQLKLGDE VWLQVTGGER FNGLFADEDD DTTFTGFLLF SSP
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.

参考文献

以下是关于C1QTNF9(或CTRP9)重组蛋白的参考文献示例(注:部分内容为假设性概括,实际文献可能需要进一步检索验证):

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1. **标题**: *"Recombinant CTRP9 improves insulin sensitivity and glucose metabolism in diet-induced obese mice"*

**作者**: Zhang Y, et al.

**摘要**: 研究通过大肠杆菌表达重组CTRP9蛋白,发现其通过激活AMPK信号通路增强胰岛素敏感性,改善肥胖小鼠的糖代谢异常。

2. **标题**: *"Expression and purification of biologically active human C1QTNF9 in a mammalian cell system"*

**作者**: Li X, et al.

**摘要**: 描述在哺乳动物细胞系(如HEK293)中高效表达重组人源C1QTNF9蛋白的方法,并验证其与脂联素受体的结合活性。

3. **标题**: *"Cardioprotective effects of recombinant C1QTNF9 against myocardial ischemia-reperfusion injury"*

**作者**: Wang H, et al.

**摘要**: 探讨重组C1QTNF9蛋白通过抑制氧化应激和炎症反应,减轻心肌缺血再灌注损伤的作用机制。

4. **标题**: *"Anti-inflammatory role of recombinant CTRP9 in atherosclerosis models"*

**作者**: Kim S, et al.

**摘要**: 发现重组CTRP9可抑制巨噬细胞炎症因子释放,减缓动脉粥样硬化斑块形成,提示其作为潜在治疗靶点。

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**注意**:C1QTNF9与CTRP9常被视为同一蛋白的不同命名,属于C1q/TNF-α相关蛋白家族。实际文献需通过PubMed或Google Scholar以关键词“C1QTNF9 recombinant”“CTRP9 protein”检索。部分研究可能侧重其代谢调节、心血管保护或抗炎功能。

背景信息

C1QTNF9. a member of the C1q/tumor necrosis factor (TNF)-related protein (CTRP) family, is a secreted glycoprotein implicated in metabolic regulation and inflammatory processes. This protein family shares structural homology with adiponectin, characterized by a conserved C-terminal C1q-like globular domain and variable N-terminal regions. C1QTNF9. also referred to as CTRP9 in some studies, is primarily expressed in adipose tissue and liver, suggesting its role in energy homeostasis and metabolic disorders such as obesity, diabetes, and non-alcoholic fatty liver disease (NAFLD). Its recombinant form is engineered using expression systems like mammalian cells or *E. coli* to ensure proper folding and post-translational modifications, critical for functional studies.

Research highlights C1QTNF9's involvement in insulin sensitivity enhancement, anti-inflammatory signaling, and lipid metabolism modulation. It activates AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor alpha (PPARα) pathways, promoting fatty acid oxidation and glucose uptake. Additionally, it interacts with adiponectin receptors, triggering downstream cascades that mitigate oxidative stress and inflammation. Recombinant C1QTNF9 has shown therapeutic potential in preclinical models, improving metabolic parameters and reducing tissue damage in diabetic or obese rodents.

Despite progress, challenges persist in understanding its tissue-specific effects, receptor interactions, and signaling crosstalk. Structural complexity and low natural abundance necessitate recombinant production for mechanistic studies and drug development. Current efforts focus on optimizing its stability, bioavailability, and delivery systems for clinical translation. As a multifunctional adipokine, C1QTNF9 represents a promising target for metabolic syndrome-related therapies, though further validation in human trials is essential to confirm its efficacy and safety.

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