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rb phosphorylation
相关语句
  rb磷酸化
     The aberrant Rb phosphorylation might contribute to the decreased transcription of E2F downstream genes.
     这种ERK不依赖的Rb磷酸化可能是导致E2F调控的基因转录下调的原因之一。
短句来源
     The results showed that the expression of survivin and Rb phosphorylation was higher than that without LMP1 expression and LMP1 expression triggered the translocation of survivin into the nucleus and Rb phosphorylation.
     结果发现 ,LMP1表达介导survivin核移位 ,促进细胞Rb磷酸化增加 ,S期细胞数显著增加 ;
短句来源
     Studies on the state of Rb phosphorylation revealed there were two types of Rb phosphorylation in cell cycle: ERK-dependent and ERK-independent phosphorylation.
     对Rb磷酸化状态的研究显示细胞中可能存在两种不同性质的Rb磷酸化:ERK依赖的和ERK不依赖的磷酸化。
短句来源
     In normal cells, the ERK-dependent Rb phosphorylation was predominant, while in early-G1 treated CHO cells the ERK-independent Rb phosphorylation prevailed.
     正常细胞中前者占主导作用,而早G1期TC处理的细胞中后者成为Rb磷酸化的主要形式。
短句来源
     The results suggest that the colon carcinoma is associated with the decrease of p16/CDK4 complex,the decreased inhibition of Rb phosphorylation and enhance of differentiation and proliferation of cells. 
     推测结肠癌变与p16/CDK4复合物降低,对Rb磷酸化抑制减少,使细胞分裂增殖增加有关。
短句来源
  rb蛋白的磷酸化
     Taken together,the data indicate that induction of gastric cancer cells arrest in G 1/G 0 by ATRA was probably through up regulation of p21 waf1/cip1 ,which contributed to inhibition of CDK 2 and CDK 4 activities,then led to Rb phosphorylation chenges,associated with inhibition of c myc expression.
     由此证实 ,ATRA诱导胃癌细胞滞留于 G1/G0 期与其上调 p2 1 waf1/ cip1的表达和抑制CDK2 和 CDK4 激酶活性 ,进而抑制 Rb蛋白的磷酸化和 c- myc的表达有关 .
短句来源
  “rb phosphorylation”译为未确定词的双语例句
     Rb phosphorylation at G1-S transition is driven by Cdks Cdk4 and Cdk6, in protein complexes with cyclinD1 which contains nuclear localization signals and target the Ckd4/Cdk6 to the nucleus.
     在G1-S期CDK家族,主要是CDK4和CDK6与包含有细胞核位置信息的细胞周期素D1(cyclinD1)形成的复合体后磷酸化Rb蛋白家族,使Rb蛋白持续处于磷酸化状态,并且失去抑制细胞增殖的功能。
短句来源
     D-type cyclin (cyclinD, CycD) regulates the G1/S transition. Under the stimulation of the exogenous signals, CycD accumulates and binds to cyclin dependent kinase (CDK) to form active complexes, which phosphorylate the retinoblastoma (Rb) protein. Rb phosphorylation results in releasing the transcription fac- tor E2F and thereby drives the G1/S transition.
     D型细胞周期蛋白(cyclinD,CycD)调控着细胞周期G1/S的转换,基本过程为CycD在外界环境刺激下积累,并与周期蛋白依赖激酶(cyclin-dependentkinase,CDK)形成有活性的激酶,促进成视网膜细胞瘤蛋白(retinoblastoma,Rb)磷酸化,使E2F因子释放,由此促使G1/S转换,这一调控系统在高等真核生物中具有很高的保守性。
短句来源
     All these results indicated that LMP1 promoted Rb phosphorylation, cell cycle entry and triggered cell proliferation via activating survivin expression. The expression of survivin triggered by LMP1 could promote cell proliferation and inhibit cell apoptosis.
     结果提示 ,EB病毒LMP1通过survivin促进细胞增殖和抑制细胞凋亡
短句来源
     Conclusion These data suggested that atRA had antiproliferative activity by modulating G1/S cell cycle regulators and by inhibition of Rb phosphorylation in MEPM cells, which might account for the pathogenesis of cleft palate induced by retinoic acid.
     结论atRA对腭器官发育敏感期腭间质细胞增殖活力及细胞周期的抑制作用可能是atRA诱导诱导唇腭裂的机制之一。
短句来源
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  rb phosphorylation
As Rb phosphorylation is regulated by G1 cyclin dependent kinase and CDK inhibitor p27kip1, which is an important regulator of the mammalian cell cycle, we estimated the amount of p27kip1 levels by western blotting.
      
NAC and GEE also abolished the decease in Rb phosphorylation by ACA.
      
No correlation of p16 expression with clinical stage, HER2/neu immunostaining, Rb expression or Rb phosphorylation was found.
      
However, etoposide treatment led to hypo-phosphorylation of Rb, while serum withdrawal did not alter the Rb phosphorylation pattern.
      
The experiments supporting G1-phase-specific Rb phosphorylation and the historical development of this idea are reviewed.
      
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he expressions of p16,CDK4 and Rb protein were detected by immunoperoxidase paint in routine formalin fixed paraffin embedded colorectal tissue section from colorectal carcinoma,polyp and colitis.The expression of p16 was declined with the decrease of cellular differentation levels,and p16 expression in colitis was higher than that of the colorectal carcinoman and polyp.The expression of Rb in carcinoma and polyp was obviously decrease.The expression of CDK4 in the three kinds of tissue was of...

he expressions of p16,CDK4 and Rb protein were detected by immunoperoxidase paint in routine formalin fixed paraffin embedded colorectal tissue section from colorectal carcinoma,polyp and colitis.The expression of p16 was declined with the decrease of cellular differentation levels,and p16 expression in colitis was higher than that of the colorectal carcinoman and polyp.The expression of Rb in carcinoma and polyp was obviously decrease.The expression of CDK4 in the three kinds of tissue was of no significant differences.The results suggest that the colon carcinoma is associated with the decrease of p16/CDK4 complex,the decreased inhibition of Rb phosphorylation and enhance of differentiation and proliferation of cells.

采用免疫组化法分析60例结肠癌、结肠息肉及结肠炎标本Rb、CDK4和p16的蛋白表达。p16表达随细胞分化程度降低而减少,结肠炎组织p16表达随细胞分化程度降低而减少,结肠炎组织p16表达高于癌和息肉组。Rb在癌组织和息肉组织中表达明显减少。CDK4在三种病变组织中表达无显著差异。推测结肠癌变与p16/CDK4复合物降低,对Rb磷酸化抑制减少,使细胞分裂增殖增加有关。

The roles of CDKs and CDIs in regulation of cell cycle progression of human gastric cancer cells was investigated.The results demonstrated that ATRA(all trans retinoic acid) inhibited growth of gastric cancer cells through inducing cells arrest in G 1/G 0.Western blotting showed that p21 waf1/cip1 was up regulated by ATRA in gastric cancer cells,which resulted in a decreased CDK 2 activity,as revealed by immunoprecipitation assay.However,p16 ink4 ,which specifically inhibited cyclinD 1/CDK...

The roles of CDKs and CDIs in regulation of cell cycle progression of human gastric cancer cells was investigated.The results demonstrated that ATRA(all trans retinoic acid) inhibited growth of gastric cancer cells through inducing cells arrest in G 1/G 0.Western blotting showed that p21 waf1/cip1 was up regulated by ATRA in gastric cancer cells,which resulted in a decreased CDK 2 activity,as revealed by immunoprecipitation assay.However,p16 ink4 ,which specifically inhibited cyclinD 1/CDK 4 complexes,was down regulated by ATRA both at mRNA and protein levels.By accompanying with another inhibitor p21 waf1/cip1 ,it led to the increase of CDK 4 activity after treatment of ATRA for 12 h,and the decrease after 24 h.As a result,Rb protein could be regulated in its phosphorylation state by ATRA.Furthermore expression of c myc was suppressed by ATRA.Taken together,the data indicate that induction of gastric cancer cells arrest in G 1/G 0 by ATRA was probably through up regulation of p21 waf1/cip1 ,which contributed to inhibition of CDK 2 and CDK 4 activities,then led to Rb phosphorylation chenges,associated with inhibition of c myc expression.Rb might be a downstream effector of ATRA in inhibition of gastric cancer cell growth.In addition,the function of p16 ink4 might be lost in gastric cancer cells.

研究 CDKs和 CKIs在调节胃癌细胞周期进程中的作用表明 ,全反式视黄酸 ( ATRA)通过诱导细胞滞留在 G1/G0 期而抑制胃癌细胞生长 .Western blot分析显示 ,ATRA可上调 p2 1 waf1/ cip1的表达 ,而抑制 p1 6ink4 的表达 .免疫沉淀及活性测定表明 ,CDK2 激酶活性可被 ATRA抑制 ,而CDK4 活性先被诱导上升 ,2 4 h后逐渐下降 .另外 ,ATRA可以调节 Rb蛋白的磷酸化和 c- myc蛋白的表达 .由此证实 ,ATRA诱导胃癌细胞滞留于 G1/G0 期与其上调 p2 1 waf1/ cip1的表达和抑制CDK2 和 CDK4 激酶活性 ,进而抑制 Rb蛋白的磷酸化和 c- myc的表达有关 . Rb蛋白是 ATRA抑制胃癌细胞生长的下游调节因子 .另外 ,p1 6ink4 的功能在胃癌细胞中可能丧失 .

To probe the molecular mechanism of EB virus latent membrane protein 1 triggering pleiotropic biological effect of apoptosis and cell proliferation, the sub cellular distribution of survivin, the phosphorylation level of Rb, cell cycle, apoptosis and cell proliferation were detected using indirect immunofluoresence assay, gene transfection, Ab knock out, colony formation, flow cytometry, caspase 3 assay and Western blotting. The results showed that the expression of survivin and Rb phosphorylation...

To probe the molecular mechanism of EB virus latent membrane protein 1 triggering pleiotropic biological effect of apoptosis and cell proliferation, the sub cellular distribution of survivin, the phosphorylation level of Rb, cell cycle, apoptosis and cell proliferation were detected using indirect immunofluoresence assay, gene transfection, Ab knock out, colony formation, flow cytometry, caspase 3 assay and Western blotting. The results showed that the expression of survivin and Rb phosphorylation was higher than that without LMP1 expression and LMP1 expression triggered the translocation of survivin into the nucleus and Rb phosphorylation. The phosphorylation level of Rb was decreased when anti sense survivin was induced into Tet on LMP1 HNE2 by the gene transfection. The number of cells in S stage of cell cycle was decreased when survivin translocation into nucleus was blocked using Ab knock out and transcription of survivin was blocked using gene transfection. Low level expression of LMP1 could increase cell proliferation, which could be inhibited by anti sense survivin. Survivin triggered by LMP1 blocked caspase 3 activation and inhibited apoptosis. All these results indicated that LMP1 promoted Rb phosphorylation, cell cycle entry and triggered cell proliferation via activating survivin expression. The expression of survivin triggered by LMP1 could promote cell proliferation and inhibit cell apoptosis.

利用间接免疫荧光、基因转染、抗体剔除 (Ab knock out)、细胞平板集落形成、流式细胞术以及半胱氨酸天冬酰胺酶 (caspase3)活性检测等方法 ,从survivin核移位、Rb磷酸化、细胞周期演进、细胞克隆形成和细胞凋亡等方面 ,探讨EB病毒潜伏膜蛋白 1(LMP1)调控细胞增殖和细胞凋亡双重效应的分子机制 .结果发现 ,LMP1表达介导survivin核移位 ,促进细胞Rb磷酸化增加 ,S期细胞数显著增加 ;LMP1通过survivin促进细胞克隆形成 .用Ab knock out阻断survivin核移位和survivin反义核酸抑制survivin表达时 ,Rb磷酸化水平降低 ,S期细胞减少 ,抑制LMP1介导的细胞增殖 ,活化细胞caspase 3,诱导细胞凋亡 .结果提示 ,EB病毒LMP1通过survivin促进细胞增殖和抑制细胞凋亡

 
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