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However, because acetylation and methylation are driven by cell signals, the epigenome is dynamic, enabling it to respond to the environment.

但是,因为乙酰化和甲基化是通过细胞信号驱动的,表观组是动态的,使得它能够对环境进行反应。

There is abnormally high uptake of 11-C-choline in a lung tumor, and the activities of both ChAT and ChoK are increased in cells of lung cancer.

肺癌的胆碱显像有异常增高,其增高原因与肺癌细胞中胆碱代谢的磷酸化途径及乙酰化途径增高有关。

We found that NaBu stimulated ALAS2 gene expression not only in erythroid K562 cells, but also in non-erythroid 293T cells with a concurrent increase in acetylation level of histone H3 and dimethylation level of K4 at the same histone at ALAS2 gene promoter.

同时ALAS2基因启动子的组蛋白H3乙酰化水平以及组蛋白H3的第4位赖氨酸的双甲基化水平升高。

METHODS: Fresh bovine tendo calcaneus collagen was dispersed in 0.5 mol/L acetic acid, co-precipitated with chitosan and lyophilized. Dry membranes were cross-linked in 0.05% glutaraldehyde for 24 hours. In vitro its degrading rate was measured by use of collagenase degrading test. The chitosan-collagen membrane was implanted to subcutaneous dorsal sites of SD rats. After implantation, histocompatibility, vascularity and degradation were observed in vivo.

以酸溶法制备胶原溶液,添加一定比例的脱乙酰化几丁质,冻干成膜,0 。0 5 %戊二醛溶液浸泡交联,行体外酶降解实验,检测其耐受酶降解能力;将制备的几丁质-胶原蛋白膜包埋于 36只 SD大鼠皮下,术后 3、5天,1、2、3、4、6、8和 12周取材,检测其组织相容性、血管化能力及材料在体内降解情况。

This result provided the reference for adjusting dosage regimen of the drug subjected to the metabolism of demethylation and acetylation for clinic.

可为临床调整经去甲基化、乙酰化代谢药物的用药方案提供参考依据。

We have investigated whether the combination of decitabine and a clinically relevant inhibitor of histone deacetylase activity (belinostat, PXD101) can further increase the re-expression of genes epigenetically silenced by DNA methylation and enhance chemo-sensitisation in vivo at well-tolerated doses.

我们研究了地西他滨联合组蛋白去乙酰化酶抑制剂(belinostat,PXD101)是否可以进一步增加DNA甲基化后生沉默基因的重新表达,在耐受性良好的剂量下增加化疗敏感性。

Such changes in thiols by allyl sulfurs may also account for the observed hyperphosphorylation of specific cell cycle proteins and the histone hyperacetylation that has been correlated with suppressed tumor cell proliferation.

这些烯丙基硫化物引起的硫醇的改变同时也可以使特异性细胞周期蛋白过磷酸化及组蛋白过乙酰化,从而抑制肿瘤细胞增殖。

Some stimulators, including viruses, tumor cells and hot shock, could promote the expression of NKG2 receptors and their ligands via activating certain transcription factors which are capable of up-regulating NKG2 promoters' activity. Meanwhile, epigenetic mechanisms including DNA methylation and histone posttranslational modifications are also critical to expression of NKG2 receptors and their ligands and may control the clonally distribution of some NK cell receptors.

病毒、肿瘤和热休克等刺激可以通过激活相应的转录调节因子,提高启动子活性而上调NKG2家族受体及其配体的表达,而启动子区DNA的甲基化状态、组蛋白的乙酰化和甲基化等表观遗传调控,在NK细胞受体及其配体的表达方面亦起重要作用,并决定NK细胞受体的克隆性分布。

Furthermore, proton singlets of Fmoc group were treated as internal standard because of their station in both starting material and product.

用HR/MAS NMR分析技术不仅跟踪优化了固相羟基氨基酸的糖基化反应条件,而且选择固载在树脂上的糖基化Nα-Fmoc保护羟基氨基酸〓H NMR中最低场,且分辨好的Fmoc保护基信号做为内标,糖上乙酰基的积分面积为标准直接定量了键合在Tenta Gel S NH〓树脂上氨基酸甙化的产率。

The increasing singlets of protons from acetyl group of product were treated as a reporter of the reaction progress. The reaction yields are calculated by the HR/MAS NMR.

利用四个羟基未保护的Nα-Fmoc氨基酸和七种全乙酰化糖为原料,合成了28个糖基化Nα-Fmoc氨基酸,均用高分辨魔角核磁共振技术定量。

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