首页> 外文期刊>Endocrine journal >cDNA Cloning and Chromosomal Mapping of Rat Smad2 and Smad4 and Their Expression in Cultured Rat Articular Chondrocytes
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cDNA Cloning and Chromosomal Mapping of Rat Smad2 and Smad4 and Their Expression in Cultured Rat Articular Chondrocytes

机译:大鼠Smad2和Smad4的cDNA克隆和染色体定位及其在大鼠关节软骨细胞中的表达。

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References(23) Cited-By(2) Smad proteins are known to transduce signalling of TGF-β receptor superfamily. We report here the entire sequences of rat Smad2 and Smad4 which have not been identified yet. Entire sequences were identified by degenerated polymerase chain reaction and following phage library screening and 5' RACE. The predicted amino acid sequences of rat Smad2 and Smad4 are highly conserved among rat, human and mouse. We also mapped these Smads to chromosome 18q.12.3. Unlike endothelial cells, TGF-β1 stimulates articular chondrocyte proliferation as well as extracellular matrix production, and acts as a repairing agent against cartilage destruction. Since both Smad2 and Smad4 are essential factors for TGF-β signalling, we examined their expression and regulation in cultured articular chondrocytes. Northern blot analysis showed that TGF-β1 significantly increased the mRNA level of Smad2 but not of Smad4 in a dose- and time-dependent manner, suggesting that the augmentation of TGF-β1 action is caused by increasing the expression of the downstream signalling molecule.
机译:参考文献(23)被引用的By(2)Smad蛋白可转导TGF-β受体超家族的信号传导。我们在这里报告尚未鉴定的大鼠Smad2和Smad4的完整序列。通过简并的聚合酶链反应并通过噬菌体文库筛选和5'RACE鉴定整个序列。大鼠Smad2和Smad4的预测氨基酸序列在大鼠,人类和小鼠中高度保守。我们还将这些Smads映射到染色体18q.12.3。与内皮细胞不同,TGF-β1刺激关节软骨细胞的增殖以及细胞外基质的产生,并充当软骨破坏的修复剂。由于Smad2和Smad4都是TGF-β信号转导的必需因子,因此我们检查了它们在培养的关节软骨细胞中的表达和调控。 Northern印迹分析表明,TGF-β1以剂量和时间依赖性方式显着增加Smad2的mRNA水平,而不是Smad4的mRNA水平,表明TGF-β1作用的增强是由下游信号分子的表达增加引起的。

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