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甲基化作用

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As an important transcription factor, methyl-CpG binding domain protein1 (MBD1) mediated transcription-suppressing course and might cause descentexpression of numerous tumor suppressor genes, or even result in devitalization ofthose genes.

作为一个重要的转录调控因子,胰腺癌中甲基化 CpG 结合域蛋白 1(methyl-CpG binding domain protein 1 ,MBD1)介导的甲基化转录抑制作用可能是造成众多抑癌基因转录表达下降,以至失活的重要原因。

Objective To detect the expression of CD70 in peripheral T lymphocytes of patients with systemic lupus erythematosus and the effect of azacitidine, an inhibitor of DNA methylation, on it. Methods Blood samples were obtained from 10 patients with active SLE (SLEDAI score ≥5), 10 patients with nonactive SLE (SLEDAI score 5) and 10 normal human controls.

目的 通过研究共刺激分子CD70在SLE患者外周血T淋巴细胞的表达水平,以及DNA甲基化抑制剂氮杂胞苷对正常人外周血T淋巴细胞表达CD70分子的影响,探讨DNA甲基化在SLE患者外周血T淋巴细胞表达CD70分子中的调控作用。

Furthermore, besides considering changes in DNA methylation as mechanisms of disease, the role of epigenetics in general and DNA methylation in particular in transgenerational carcinogenesis, in memory formation and behavior establishment are brought about as mechanisms based on the cellular memory of gene expression patterns.

而且,除了考虑DNA甲基化改变作为疾病的机制外,表观遗传学一般的及DNA甲基化特别的在隔代致癌中的作用,在记忆形成和行为确立被引发作为基于基因表达模式的细胞记忆的机制。

After the carboxymethylation,the solubility of pachyman in the water was significantly increased,its β-D-glucan characteristic absorption peak at 890 cm-1 became weak obviously,and its methylene vibration absorption peak and CO antisymmetrical stretch vibration absorption peak appeared at 1 333 and 1 606 cm-1 respectively,which indicated that the carboxymethylation succeeded.The analysis of AFM results showed that CMP molecules existed in different morphology under different solution conditions,and that the concentration,ionic strength and solvent physical chemistry characteristics of polysaccharide solution had effects on the CMP chains conformation and the action mode between different molecular chains.The phenomena were considered to be related to hydrogen bond association and intramolecular and intermolecular electrostatic interactions of CMP.

结果表明:经过羧甲基修饰,茯苓多糖在水中的溶解性显著增加,890 cm-1 处的β-D-葡聚糖特征吸收峰明显减弱,1 333 cm-1 处出现次甲基振动吸收峰,1 606 cm-1 处出现〖JG(〗C〖ZJLX,Y〗O〖JG)〗非对称伸缩振动吸收峰,表明羧甲基化成功;原子力显微镜分析表明:在不同溶液条件下,CMP分子以不同形态存在,多糖溶液的浓度、离子强度及溶剂的物化特性均能对CMP的分子链构象及链间相互作用形式产生影响,推测可能与CMP分子内、分子间的氢键缔合及静电作用有关,CMP分子与云母基底间的吸附及静电作用也会对CMP的分子链构象及图像质量产生影响。

To find methylated genes, researchers usually turn to a technique called bisulphite sequencing, which chemically changes normal cytosine to thymidine (T; another DNA base), while leaving methylated cytosines unchanged.

研究者通常借助于亚硫酸氢盐测序技术检测甲基化的基因,它通过化学反应使正常胞嘧啶转变为胸腺嘧啶,而对甲基化的胞嘧啶无作用。

Ethylation specific PCR analysis also revealed that the BLU promoter was highlymethylated in 74%(17 of 23) of primary tumors where the gene was downregulated,whereas only 2 of 9 non-neoplastic nasopharyngeal epithelia exhibitedhypermethylation in the BLU promoter region.

SP分析的结果表明,在23例表达下调的鼻咽癌组织中,17例(74%,17/23)标本的BLU基因发生了异常甲基化,而9例非癌对照中仅有2例甲基化,说明启动子甲基化在BLU基因的转录失活中具有重要作用。

Inhibition of SAHH has been known to result in accumulation of intracellular levels of AdoHcy, which is a potent inhibitor of all S-adenosyl-L-methionine-dependent transmethylation reactions.

抑制SAHH将导致细胞内甲基化抑制物AdoHcy的堆积,从而时转甲基反应产生反馈性抑制作用。而甲基化对于维持细胞的活性是必需的。

Inhibition of SAHH has been known to result in accumulation of intracellular levels of AdoHcy, which is a potent inhibitor of all S -adenosyl- L -methionine-dependent transmethylation reactions.

抑制SAHH将导致细胞内甲基化抑制物AdoHcy的堆积,从而对转甲基反应产生反馈性抑制作用。而甲基化对于维持细胞的活性是必需的。

In this thesis, based on a recent genome-scale dataset of DNA methylation in human brain tissues, we developed a classifier for predicting methylation status of CpG islands using a Support Vector Machine. Nucleotide sequence contents, transcription factor binding sties and Alu repeats are used as features for the classification. The method achieves accuracy of ~85% on the brain data.

本文的主要工作就是基于人脑测得的DNA甲基化数据,挖掘DNA序列特征,用支持向量机的方法实现了预测CpG岛甲基化的目标,得到了85%的预测正确率,同时还验证了所选的三类特征对于CpG岛甲基化的指导作用,它们分别是DNA序列组合、转录因子结合位点TFBS和短重复序列Alu。

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。

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