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And cell cycle was arrested of G0/ G1 phase. 并且将细胞周期阻滞于G0/G1期。
Rapamycin arrested cell cycle in G1 phase to antitumor by degrading the CDK-cyclin complexes kinase activity. Rapamycin 还能通过降低CDK-cyclin 复合物激酶的活性,使细胞周期阻滞在G1期,从而发挥抗肿瘤的作用。
The ratio of G1 phase of CaSki-S cell was increased and the ratio of S phase was decreased. 流式细胞仪检测细胞周期显示,CaSki-S细胞与未转染组CaSki细胞比较,G1期细胞比例明显增加,S期细胞比例则明显减少。
If left unrepaired during G1 phase, bulky DNA lesions can block DNA polymerases. 如果损伤在G1期没有得到修复，那么大片段损伤会阻碍DNA聚合酶结合。
Chemical alterations of nucleotide bases are often removed by BER, as in G1 phase. 碱基的化学修饰通常在G1阶段由BER去除。
CLT can induce apoptosis in vitro in human colon cancer cell line CCL 229.The apoptosis inducing effect may be G1 phase specific. 克霉唑对人结肠癌细胞系CCL229有明显的凋亡诱导作用,并且能特异地诱导G1期细胞凋亡。
ATO and STI571 both could make K562 cells arrest in G2/M phase, and the number of cells in G1 phase and S phase decreases significantly. ATO和STI571均可诱导K562细胞凋亡，细胞周期检测示G_1、S期细胞减少，细胞阻滞于G_2/M期。
After transfection with pcDNA3-p21, the proliferation of cultured BGC was significantly inhibited and cells in G1 phase were resisted. p21导入胃癌BGC细胞后,肿瘤细胞增值能力明显受到抑制,并出现细胞周期G1期阻滞。
Both NPPB (100 umol/L) and TAM (10 umol/L) can increase DNA level of G1 phase and decease that of S phase significantly. NPPB(100林mol/L)和TAM(10林mol几)均可提高人胃策四军医大月卜祠叹士学位论文
Nucleotide-excision repair (NER) plays an important role during G1 phase to remove bulky lesions, such as those caused by ultraviolet irradiation. 核苷酸切除修复在G1期去除像紫外照射引起大片段损伤时发挥非常重要的作用。
With the increase in EPO concentration, the percentage of cells in G1 phase gradually decreased, but increased in S+G2/M phase cells. 随促红细胞生成素浓度的升高，G1期细胞所占百分率逐渐降低，而S+G2/M期细胞所占百分率逐渐升高。
The ratio of apoptosis was 28.2% when treated with 4000ug/ml RTE for 48hr and the cells were inhibited in G1 phase, and cells in G1/G0 phase were significantly increased. 用流式细胞仪分析表明：4000ug/ml附子提取物作用48hr后，CEM细胞凋亡率可达28.;2%25，CEM细胞被阻止于G1期，G1/G0期细胞明显增多。
The S phase cells has a lower adhesion forces than the G1 phrase under the synchronized disposition. This may reflects the active biochemical reactions in the cells in G1 phase. 同步化处理后S期HCC细胞与胶原IV的粘附力较G1期小，分析这可能与G1期有较活跃的胞质化学反应相关联。
For the cell cycle, the percentage of G0 and G1 phase cells in hypoxia group were lower than in normal group, whereas the percentage of S phase cells higher. 细胞周期中，处于G0、G1期的细胞百分值，低氧组较常氧组低，但S期细胞百分值升高。
It was found that wild-type gene PTEN could suppress the proliferation of hepatocellular carcinoma cells and induce G1 phase block wile the mutated PTEN gene lost this function. 本课题最后发现野生型PTEN基因可抑制肝癌细胞的增殖，诱导G1期阻滞；而突变的PTEN基因无上述作用。
The results showed that: upon stimulated by serum, the mRNA expression of c-ski began to increase and reached the highest level at G1 phase peak, then declined at S phase, and sustained low expression at G2/M phase. 结果显示:c-skimRNA表达在加入血清后开始升高,在细胞周期G1期的高峰期达到峰值,S期显著下降,在G2/M期维持在较低的水平;
Cyclin D3 is found to play a crucial role not only in progression through the G1 phase as a regulatory subunit of CDK 4 and CDK 6, but also in many other aspects, such as cell growth, cell differentiation, transcriptional regulation and apoptosis. 在cyclin D中,cyclin D3不仅作为一个CDK4和CDK6的调节亚基在G1期调节细胞周期进程,还与细胞生长、细胞分化、转录调节和凋亡有关。
The factors that regulate the cell cycle include Cyclin, Cyclin-dependent kinase(CDK), Cyclin-dependent kinase inhibitor(CKI). CyclinDl is the major control switches in the G1 phase. 参与细胞周期调控的蛋白主要有：细胞周期蛋白(Cyclin)、细胞周期蛋白依赖性激酶(Cyclin-dependent kinase，CDK)、细胞周期蛋白依赖性激酶抑制因子(Cyclin-dependent kinase inhibitor，CKI)。
The G1 phase of cell cycle was arrested by DAC combined with TSA,which,however,did not occur when DAC or TSA was used alone. The proportion of cells in G2 phase was increased with TSA alone. 单用DAC或TSA对细胞G1期无影响,单用TSA使G2/M期细胞比例增高,联合用药发生明显的G1期阻滞。
The MNF at Sphase of cells is obviously lower than at G1.This result suggests that most of the micronucleated cells att G1 phase do not enter Sphase and micronucleus rarely form at S phase of cells. S期细胞的MNF校G1期有极显著的下降，这提示大部分G1期的微核细胞不能进入S期，使细胞增殖中止，这可能是抗癌药物杀伤肿瘤细胞的机制之一。