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rb磷酸化
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  rb phosphorylation
     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。
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     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
  phosphorylation level of rb
     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.
     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 .
短句来源
  “rb磷酸化”译为未确定词的双语例句
     The expression of p16 lnk4a, a cell cycle inhibitory protein, was elevated and the phosphory lated RB protein was decreased in the cells treated with Deshikang as compared w ith the non-treated control cells.
     用药组p16lnk4a蛋白表达增高,Rb磷酸化蛋白表达降低,伴有非磷酸化Rb蛋白的相应增多;
短句来源
     The loss of the ability of inhibiting the cell growth resulting from the decrease or phosphorylation of Rb induced by the overexpression of cyclin-D1 might contribute to the etiology of parathyroid adenoma.
     cyclin-D1过度表达导致Rb磷酸化或表达下调而失去细胞抑制效应可能为甲状旁腺腺瘤发生的机制之一。
短句来源
     But has no effect on the expression of p16,p21. Conclusions It was seemed that EGF might down-regulate the expression of P27 and then lead to the change of CDK2、Rb and phosphorylated-Rb’s level by activating downstream signal pathway,and thereby promoted the proliferation ability in DU145 cells.
     结论EGF刺激导致其下游的信号通路活化,降低p27表达,并导致下游CDK2、Rb及Rb磷酸化水平的变化,最终促进了DU145细胞的增殖能力。
短句来源
     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.
     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 .
短句来源
     Conclusions:Our results indicated that low expression level of p27 lead to the increased proliferation ability of 95D cells, which might reflec t the progression of human lung cancer cells in cell cycle facets.
     结论:p27表达的不同,以及下游CDK2,Rb及Rb磷酸化水平的差异,最终引起两株细胞在细胞周期和细胞增殖能力的差异。
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  rb phosphorylation
Rb phosphorylation is mediated by cyclin-dependent kinases (CDKs), whose activity is enhanced by cyclins and inhibited by CDK inhibitors.
      
Although one mechanism for its tumor suppression may be prevention of Rb phosphorylation, thereby causing G1 arrest, many normal cell types express p16INK4A, and are still able to traverse the cell cycle.
      
The INK4a/ARF locus on chromosome 9p21 encodes two gene products that are involved in cell cycle regulation through inhibition of CDK4-mediated RB phosphorylation (p16INK4a) and binding to MDM2 leading to p53 stabilization (p14ARF).
      
Rb phosphorylation was more rapid in MCF-7 cells than in MCF10A cells, whereas Rb dephosphorylation appeared deregulated in MDA-MB-231 cells.
      
Antineoplaston caused the down-regulation of PKCα protein expression, resulting in inhibition of ERK MAPK phosphorylation, with resultant inhibition of Rb phosphorylation leading to G1 arrest.
      
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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 no significant...

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。

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...

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

Objective To study the relationship between COX 2 expression in esophageal cancer cell (EC/CUHK 1) and mitomycin C (MMC) treatment Methods 2 mg/L of MMC was added to the well grown EC/CUHK 1 cells cultured in RPMI 1640 including 10% FCS, and the medium was totally changed after 0 5, 1, 2, 4 and 8 h treatment, respectively Cells were collected after another 24 h culture Protein expression of COX 2, Bcl 2, Rb, p53 were examined by Western blot, and RT PCR method was used to confirm the COX 2...

Objective To study the relationship between COX 2 expression in esophageal cancer cell (EC/CUHK 1) and mitomycin C (MMC) treatment Methods 2 mg/L of MMC was added to the well grown EC/CUHK 1 cells cultured in RPMI 1640 including 10% FCS, and the medium was totally changed after 0 5, 1, 2, 4 and 8 h treatment, respectively Cells were collected after another 24 h culture Protein expression of COX 2, Bcl 2, Rb, p53 were examined by Western blot, and RT PCR method was used to confirm the COX 2 expression in mRNA level Cell cycle analysis for cells collected at 0, 0 5, 2, 4 and 8h was performed on an EPICS profile analyzer Results The cell cycle analysis showed that the percentage of apoptosis cells were (4 12±0 83)%, (1 00±0 11)%, (4 32±0 99)%, (9 46±2 11)% and (31 10±3 57)%, respectively COX 2 mRNA expression were 2 60, 1 70, and 0 08 times, COX 2 protein expression were 2 0, 3 1 and 2 8 times, Bcl 2 protein were 3 6,14 0 and 12 0 times, p53 protein were 1 8, 0 5 and 0 2 times, hyperphosphorylated form Rb were 8 2, 8 4 and 6 2 times, underphosphorylated form Rb were 1 8, 0 5 and 0 2 times in 0 5, 2 and 4h after MMC treatment, respectively, as compared with the control group Conclusions The COX 2 expression showed coincidence up regulation according to the MMC induced anti apoptosis function activation in esophageal cancer cells, and the process was at least partly associated with Rb phosphorylation and p53 accumulation It is implied that COX 2 may be a protecting factor in MMC induced esophageal cancer cell apoptosis, and the use of COX 2 inhibitor as an enhancer for esophageal cancer chemotherapy may be reasonable

目的 探讨食管癌细胞环氧合酶 2 (COX 2 )表达与丝裂霉素C(MMC)处理的关系及可能机制。方法 四唑蓝法检测 2mg/LMMC处理对食管癌细胞株EC/CUHK 1生长的影响 ,流式细胞仪分析细胞周期及凋亡细胞比例 ,逆转录 PCR及Westernblot分别检测COX 2mRNA与COX 2、Bcl 2、p5 3及Rb蛋白的非磷酸化亚型 (pRb)表达。 结果 MMC处理后 0、0 5、2、4和 8h ,凋亡细胞比率分别为 (4 12± 0 83) % ,(1 0 0± 0 11) % ,(4 32± 0 99) % ,(9 4 6± 2 11) %和 (31 10±3 5 7) %。处理后 0 5、2和 4h ,COX 2mRNA相对表达量分别为处理前的 2 6 0、1 70和 0 0 8倍 ;COX 2蛋白为 2 0、3 1和 2 8倍 ;Bcl 2为 3 6、14 0和 12 0倍 ;p5 3为 1 8、0 5和 0 2倍 ;pRb为8 2、8 4和 6 2倍 ,Rb蛋白的磷酸化亚型 (ppRb)为 1 8、0 5和 0 2倍。MMC处理后COX 2mRNA、p...

目的 探讨食管癌细胞环氧合酶 2 (COX 2 )表达与丝裂霉素C(MMC)处理的关系及可能机制。方法 四唑蓝法检测 2mg/LMMC处理对食管癌细胞株EC/CUHK 1生长的影响 ,流式细胞仪分析细胞周期及凋亡细胞比例 ,逆转录 PCR及Westernblot分别检测COX 2mRNA与COX 2、Bcl 2、p5 3及Rb蛋白的非磷酸化亚型 (pRb)表达。 结果 MMC处理后 0、0 5、2、4和 8h ,凋亡细胞比率分别为 (4 12± 0 83) % ,(1 0 0± 0 11) % ,(4 32± 0 99) % ,(9 4 6± 2 11) %和 (31 10±3 5 7) %。处理后 0 5、2和 4h ,COX 2mRNA相对表达量分别为处理前的 2 6 0、1 70和 0 0 8倍 ;COX 2蛋白为 2 0、3 1和 2 8倍 ;Bcl 2为 3 6、14 0和 12 0倍 ;p5 3为 1 8、0 5和 0 2倍 ;pRb为8 2、8 4和 6 2倍 ,Rb蛋白的磷酸化亚型 (ppRb)为 1 8、0 5和 0 2倍。MMC处理后COX 2mRNA、pRb和 p5 3蛋白之间以及COX 2、ppRb和Bcl 2蛋白之间的表达改变密切相关。 结论 MMC可上调食管癌细胞的COX 2表达 ,且明显与Bcl 2过表达相关 ,p5 3及Rb磷酸化积累可能调节COX 2蛋白的表达

 
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