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Expression of type VI, IX and XI collagen genes and alternative splicing of type II collagen transcripts in fracture callus tissue in mice

机译:小鼠骨折call组织中VI,IX和XI型胶原基因的表达和II型胶原转录物的可变剪接

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>The levels of six mRNAs coding for constituent α-chains of three minor collagens of cartilage were analyzed in an experimental fracture model in normal and transgenic Del1 mice harboring a deletion mutation of exon 7 in the type II collagen gene. Reduced and retarded chondrogenesis in Del1 mice was evident in callus samples as reduced mRNA levels for the cartilage specific type IX and XI collagens at days 7 and 9 of fracture healing. Analysis of the calluses for alternative splicing of proα1(II) collagen mRNA also suggested retarded chondrogenesis in Del1 calluses. Another developmentally regulated step in limb development, a switch between alternative promoters of the α1(IX) collagen gene, was also seen during fracture healing but was less obvious in Del1 calluses. Finally, the current data suggest that the abnormality in bone remodelling in Del1 mice involves activation of the genes coding for α1(XI) and α2(VI) collagens.
机译:在正常和转基因的Del1小鼠中,在II型胶原蛋白基因中存在外显子7的缺失突变,在实验性骨折模型中分析了编码三个软骨小胶原蛋白的α链组成的六个mRNA的水平。在愈伤组织样品中,Del1小鼠的软骨形成减少和受阻很明显,因为骨折愈合第7天和第9天软骨特异性IX和XI型胶原的mRNA水平降低。分析老茧的proα1(II)胶原蛋白mRNA的可变剪接也暗示了Del1老茧中软骨形成的延迟。在骨折愈合过程中还可以看到肢体发育的另一个受发育调节的步骤,即α1(IX)胶原基因的替代启动子之间的转换,但在Del1愈伤组织中不那么明显。最后,当前数据表明,Del1小鼠的骨骼重塑异常涉及激活编码α1(XI)和α2(VI)胶原蛋白的基因。

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    《FEBS Letters》 |1995年第2期|共页
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  • 中图分类 分子生物学;
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  • 入库时间 2022-08-18 19:13:18

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