纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | TRIB3 |
Uniprot No | Q96RU7 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-358aa |
氨基酸序列 | MRATPLAAPAGSLSRKKRLELDDNLDTERPVQKRARSGPQPRLPPCLLPL SPPTAPDRAT AVATASRLGPYVLLEPEEGGRAYQALHCPTGTEYTCKV YPVQEALAVLEPYARLPPHKHV ARPTEVLAGTQLLYAFFTRTHGDMHS LVRSRHRIPEPEAAVLFRQMATALAHCHQHGLVL RDLKLCRFVFADRE RKKLVLENLEDSCVLTGPDDSLWDKHACPAYVGPEILSSRASYSGK AA DVWSLGVALFTMLAGHYPFQDSEPVLLFGKIRRGAYALPAGLSAPARCLV RCLLRREP AERLTATGILLHPWLRQDPMPLAPTRSHLWEAAQVVPDGL GLDEAREEEGDREVVLYG |
预测分子量 | 69 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TRIB3重组蛋白的3篇代表性文献,涵盖其功能及机制研究:
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1. **文献名称**:*TRIB3 regulates endoplasmic reticulum stress-induced neuronal apoptosis*
**作者**:Ord D, et al.
**摘要**:本研究通过重组TRIB3蛋白,揭示了其在阿尔茨海默病模型中调控内质网应激介导的神经元凋亡的作用。实验表明,TRIB3与CHOP蛋白相互作用,增强caspase-3活化,提示其作为神经退行性疾病的潜在治疗靶点。
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2. **文献名称**:*Tribbles homolog 3 modulates autophagy via interaction with ATG7*
**作者**:Du Y, et al.
**摘要**:该研究利用重组TRIB3蛋白进行体外结合实验,发现TRIB3通过直接结合自噬相关蛋白ATG7.抑制自噬体形成,从而促进肝癌细胞的化疗耐药性,为癌症治疗提供了新视角。
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3. **文献名称**:*TRIB3 inhibits AKT phosphorylation by competing for binding to insulin receptor substrate 1*
**作者**:Ohoka N, et al.
**摘要**:通过重组蛋白互作实验,作者证实TRIB3与胰岛素受体底物1(IRS1)结合,干扰AKT磷酸化,导致胰岛素信号通路受阻。这一机制在2型糖尿病模型中与胰岛素抵抗密切相关。
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**备注**:上述文献均涉及重组TRIB3蛋白的应用,涵盖神经疾病、癌症和代谢疾病领域。如需扩展,可进一步检索近年研究(如2020年后)聚焦TRIB3结构解析或靶向治疗的文献。
TRIB3 (Tribbles homolog 3) is a pseudokinase belonging to the Tribbles family of proteins, which play critical roles in regulating cellular stress responses, metabolic pathways, and apoptosis. Unlike typical kinases, TRIB3 lacks catalytic activity due to evolutionary modifications in its kinase domain. Instead, it functions as a scaffold or adaptor protein, modulating signaling cascades by interacting with key molecules such as AKT, MAPK, and ATF4. Its expression is induced under various stress conditions, including endoplasmic reticulum (ER) stress, nutrient deprivation, and hypoxia, positioning it as a mediator of cellular adaptation to environmental challenges.
Recombinant TRIB3 protein is engineered for research to study its interactions and regulatory mechanisms. Produced using expression systems like *E. coli* or mammalian cells, it retains functional domains necessary for binding partners, enabling *in vitro* studies on its role in insulin resistance, cancer progression, and neurodegenerative diseases. For example, TRIB3 is implicated in type 2 diabetes by interfering with insulin signaling through AKT inhibition and in cancer by promoting tumor cell survival via stress-response pathways. Its dual role as both a pro-survival and pro-apoptotic factor, depending on cellular context, makes it a compelling therapeutic target.
Research on recombinant TRIB3 also explores its potential as a biomarker for metabolic disorders or cancer prognosis. Structural studies using the recombinant protein help map interaction sites, guiding drug development to disrupt pathological TRIB3 interactions. Despite progress, its pleiotropic effects and tissue-specific functions necessitate further investigation to harness its clinical potential safely. Overall, TRIB3 recombinant protein serves as a vital tool for decoding its complex biology and translational applications.
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