Lepr<sup>em4Lizh</sup>
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The Lepr knockout mutation were generated by CRISPR/Cas9. The resulting mutaion is a 298-bp deletion from No. 90043 bp to 90341 bp in the Lepr genome DNA sequence (NC_005104.4) and a 4-bp insertion and resulted in a termination codon TGA. For genotyping, a 662-bp fragment of WT and a 368-bp fragment of the Lepr knockout gene were amplified with PCR.<br>ASSOCIATED WITH decreased bone mineral density; decreased trabecular bone volume; expanded mesangial matrix; ASSOCIATED WITH Dyslipidemias; glucose intolerance; hyperglycemia
通过CRISPR/Cas9技术构建的Lepr敲除突变体。该突变导致Lepr基因DNA序列(NC_005104.4)中第90043碱基至第90341碱基之间发生298碱基的缺失,并伴随4碱基的插入,最终导致终止密码子TGA的出现。为了进行基因分型,利用聚合酶链反应(PCR)扩增了野生型基因的662碱基片段和Lepr敲除基因的368碱基片段。该突变与降低的骨矿物质密度、减少的骨小梁骨体积、扩大的系膜基质有关,并伴随有血脂异常、葡萄糖不耐受和高血糖等病症。



