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This implies that the increase of genetranscripts is because of the positive effect of TSA on acetylation in reprogramming.

在aphicicolin单独处理组中基因的表达水平也没有显著升高,提示基因表达量的显著增加是由于TSA诱导了核重编程过程中组蛋白高度乙酰化而引起的。

On the other hand, we suggest that the STAT3-induced histone deacetylation in the IL-4 promoter may play an initial role in IL-4 suppression.

另一方面,我们认为STAT3诱导的IL-4启动子组蛋白去乙酰化在IL-4基因的抑制中发挥了起始性的作用。

The dependence of the relative intensity of cationic molecule and fragmentation ion of an acetylated melezitose on the concentration of Na + or Li + in the matrix was studied by using fast atom bombardment source .

利用快原子轰击源研究了乙酰化松三糖的阳离子化分子和碎片离子的相对强度随底物中Na+或Li+浓度变化的趋势。

We ever reported cellulose is in propyl of Xi of ionic liquid 1-- chloric salt of Zun of 3- methylic Mi (the homogeneous phase acetyl in Am ImC L) converts reaction, falling without activator condition, one pace gets the CA of different DS, get acetone but the CDA[12] of dissolve.

我们曾报道了纤维素在离子液体1-烯丙基-3-甲基咪唑氯盐中的均相乙酰化反应,在无催化剂条件下,一步得到不同DS的CA,并得到丙酮可溶的CDA[12]。

The famciclovir was synthesized from purine by a series of steps by Acylation, Decarboxylation, Reduction ,and so on; Derivatives of these intermediates is described from the 6-chloro- 9H- purin-2-amine as raw materials in different conditions when the iodine and bromide were synthesized with the addition of two intermediate 6-bromo-9H-purin-2-amine and 6-iodo-9H-purin-2-amine; There is elaborated from the main part of a acetophenone, urineaminohydrochloride, phenylhydrazine, ethyl acetoacetate as raw material through a series of reactions to synthetic 3-phenyl-4-formylphenyl pyrazole and 5-chloro-3-methyl-1-phenyl-1H-pyrazole-4-aldehyde two pyrazole aldehyde, and then with 2-amino-6-chlorine-9-(2-methicillin-oxo-co-methyl-4-yl) purine reaction of the two new pyrazole purine Schiff bases.

本论文主是采用以鸟嘌呤为原料,经过一系列的酰基化,脱羧,还原等反应作用下最终得到了产物2-氨基-9-(4-乙酰氧基-3-乙酰氧基甲基丁基)嘌呤;其中的中间体衍生物主要是阐述从以2-氨基-6-氯鸟嘌呤为原料通过在不同的条件下进行溴代与碘代分别合成了另外两种中间体2-氨基-6-溴鸟嘌呤及2-氨基-6-碘鸟嘌呤;还有一部分主要是阐述从以苯乙酮,盐酸氨基脲,苯肼,乙酰乙酸乙酯为原料通过一系列的反应先合成3-苯基-4-醛基吡唑及5-氯-3-甲基-1-苯基-1H-吡唑-4-甲醛这两个吡唑醛,然后再与2-氨基-6-氯-9-(2-甲氧羰基丁酸甲酯-4-基)嘌呤反应得到了两个新型的吡唑嘌呤席夫碱

Strikingly, neurons defective in Elongator show reduced levels of acetylated -tubulin.

令人吃惊的是,有缺陷的神经元细胞在Elongator表现了出低水平的乙酰化微管蛋白。

The synthesis of alkylcyclohexylbenzoic acid: take the synthesis of ethylcyclohexylbenzoic acid as a typical example. With the AlCl3 as the catalyst, cis+trans acetylcyclohexylbenzene is synthesized from the reaction of acetyl chloride, cyclohexene and benzene.

烷基环己基苯甲酸的合成研究:主要研究了乙基环己基苯甲酸的合成,以乙酰氯、环己烯、苯为原料,三氯化铝为催化剂,合成乙酰基环己基苯,用水合肼、氢氧化钾、一缩二乙二醇经过高温加热还原羰基(Wolff-黄鸣龙还原),将所得到的乙基环己基苯用乙酰氯进行傅克酰基化得到乙基环己基苯乙酮,所得中间体经过处理之后直接得到反式产物,将反式异构体的乙酰基氧化得到反式烷基环己基苯甲酸。

The results suggested that chitinhad a good solubility in the new solvent when its at -30℃and below, but the solubilityof chitin no longer increasesd notable as the temperature reduced; The joined of urea, incertain degree, strengthened the solvency of alkali solvent to chitin. When theconcentration of sodium hydroxide is 8%~12%, Chitin had a good solubility, and theapparent viscosity of chitin solution could up to 4000 mpa·s~5000mpa·s at roomtemperature; In addition,the solubility of chitin in new solvent was high when therefrigerated time was three days and above, but the refrigerated time could not too long,otherwise, the deacetylize degree of chitin got more bigger. The properties of chitin solution were tested by revolving viscosimeter, FT-IR,X-RD and so on.

结果表明,在-30℃及以下甲壳素能很好的溶解于新溶剂中,但甲壳素的溶解度不再随温度的下降而有所增大,而是基本保持不变;尿素的加入,在一定程度上强化了强碱溶剂对甲壳素的溶解,当新溶剂中NaOH浓度为8%~12%时,甲壳素在试验温度下可以获得较好的溶解度,所得溶液在室温下的表观黏度达4000 mpa·s~5000mp·s;冷冻时间为3 d及以上时,有利于甲壳素的溶解,超过3 d,甲壳素的溶解度变化不大,另外,冷冻条件下,甲壳素在强碱溶剂中仍会发生脱乙酰化反应,冷冻时间不宜太长。

These data suggest that histone acetylation during nuclearremodeling (from the start of activation to the formation of pronuclei) is independent fromthe event that oocyte cytoplasm inhibits the transcription of specific genes in thedifferentiated cells, but induces reprogramming of gene expression.

这表明组蛋白的乙酰化修饰可能没有参与卵细胞质对分化细胞特有的基因转录的抑制,但引起了基因表达模式的变化。

Meanwhile,HDAC1 acetylation level is significantly increased.The overexpression of HDAC1 can promote erythroid cell proliferation and inhibits induced differentiation,the knockdown of HDAC1 or 2 inhibits erythroid cell proliferation and promotes induced differentiation.We also found that HDAC1 affects GATA1 mediated transcription activity.Thus our data revealed that HDAC1 may negatively regulate GATA1 mediated transcription and suggest that the dynamic regulation of GATA1 associated NuRD/MeCP1/HDAC1/HDAC2 complex may determine the onset of erythroid differentiation programs.Moreover,this study will eventually help to design new therapeutic approaches in treatment of leukemia.

研究发现在被诱导分化的小鼠红细胞白血病细胞中与GATA1相结合的HDAC1被乙酰化并失去活性,在血细胞中过表达HDAC1能够促进血细胞的增殖并抑制分化,反之在血细胞中敲除HDAC1或HDAC2能抑制血红细胞的增殖并促进分化,而且HDAC1能够负调控GATA1的转录活性,GATA1与NuRD/MeCP1复合体之间的动态调控,决定血红细胞分化的发生和发展,并为探索白血病的致病机理奠定了理论基础。

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