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- 這是Shepen,Mut的木乃伊,她曾一度在梯比斯寺院當過(guò)歌手。The mummy is that of Shepenmut who was once a singer in the Temple of Thebes.
- 甲基丙二酸血癥患兒mut基因兩個(gè)新遺傳突變的發(fā)現和鑒證Molecular analysis of two novel mut gene mutations in chinese patient with methylmalonic academia
- 這是Shepen,Mut的木乃伊，她曾一度在梯比斯寺院當過(guò)歌手。The mummy is that of Shepenmut who was once a singer in the Temple of Thebes.
- Mut-HPI與改造前的Met-HPI相比，不易被胰酶和羧肽酶B(CPB)降解。Mut-HPI was less easily digested by trypsin and CPB than Met-HPI.
- 實(shí)驗結果表明,誘導表達48h后,Mut+和MutS重組子表達的產(chǎn)物在SDS-PAGE膠上都出現了清晰的目的帶。SDS-PAGE results indicated that there was a clear target band in Muts and Mut+ recombinant Culture supernatant after 48 hours culture respectively.
- 與Mut~+型相比，Mut~s轉化子在含營(yíng)養和色素較少的BMM培養基中即有高表達，且表達產(chǎn)物雜蛋白少，易于純化。Compared with the Mut~+, the Mut~s-hFL transformants showed higher expression level with less coloring contamination in the product and easier purification for hFL.
- 將此重組表達載體線(xiàn)性化后通過(guò)電轉化的方法轉化PMAD11酵母感受態(tài)細胞，篩選Ade~+(Mut~s)重組子并誘導表達。After the recombinant plasmid pMET-PLF-N was linearized and transformed into PMAD11 compentent cells by electroporation, Ade+(Muts)recombinants were selected and induced with methanol.
- 結果表明，誘導培養48小時(shí)后，Mut~+重組菌株表達產(chǎn)物在SDS-PAGE膠上顯現出清晰的目的蛋白帶，而Mut~s重組菌株培養72小時(shí)才能顯示微弱的目的帶；SDS-PAGE results showed that there was a clear target protein band in Mut+ recombinant supernatant after 48 hours of culturing, while a faint band only in Muts recombinant after 72 hours.
- 在含丙烯醇的YPD篩選培養基上篩選獲得兩株ADH活力降低的突變株mut-1和mut-2,檢測突變株mut-1和mut-2的最大ADH活力分別為35.67和43.09U/mL,是原始菌株的41.63%和50.29%。Two mutants,named mut-1 and mut-2,with decreased ADH activity were screened out by yeast peptone dextrose(YPD)agar medium containing allyl alcohol. These two mutants had decreased ADH activities of 41.63%25 and 50.29%25 compared with the parent strain.
- 以同樣方法獲得的Met-人胰島素原(Met-HPI)為對照，研究了其理化性質(zhì)和生物活性的變化，結果表明，Mut-HPI保留了大部分放射免疫活性，而受體結合活性卻只有Met-HPI的5.2%。It showed 78.08%25 radio immuno activity (RIA), but only about 5.2%25 of receptor binding activity (RBA) as compared with Met-human proinsulin (Met-HPI) which was prepared in the same way.
- 小干擾RNA對白血病MDR細胞系K562/A02 mdr-1轉錄、P-gp表達、P-gp功能及K562/A02細胞耐藥表型的影響，并進(jìn)行RNAi的特異性分析。 設計與si-MDR1僅有一個(gè)堿基突變的序列（si-MDR1-mut）為對照。An increase of intracellular DNR retention in si-MDR1-treated cells was observed, confirming the inhibition of P-gp function by siRNA targeted MDR1. One base pare mutated control (si-MDR1-Mut) lost the effect of si-MDR1 on both the degradation of mdr1 mRNA and the reduction of P-gp expression.
