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去B链羧端三肽人胰岛素原的基因构建和表达 总被引:1,自引:0,他引:1
用改进的寡苷酸诱导 突变法将人胰岛素原基因(BCA)删除编码B链羧端三肽的碱基片段,得到去B链羧端三肽胰岛素原的基因(B^-3CA)。为了便于表达产物的蛋白质后加工,又用PCR的方法在B链N端起始Met与Phe密码子之间增加了编码Lys的3个碱基,得到改造后基因LB^-3CA,将LB^-3CA克隆到表达质粒pBV220上,在大肠杆菌系统中热诱导表达,表达率为12%。表达产物经蛋白质后加工,得到的去 相似文献
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Chan VS Chan KY Chen Y Poon LL Cheung AN Zheng B Chan KH Mak W Ngan HY Xu X Screaton G Tam PK Austyn JM Chan LC Yip SP Peiris M Khoo US Lin CL 《Nature genetics》2006,38(1):38-46
Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection. 相似文献
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