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rb蛋白磷酸化
相关语句
  rb protein phosphorylation
     Inhibition of Cdk2 activity and decreased Rb protein phosphorylation level induced by antigen receptor crosslinking were partially reversed by the antisense oligonuceotides, leading to recovery of cell cycle progression of WEHI 231 cells.
     用p2 7Kip1反义寡核苷酸处理WEHI-2 31细胞 ,可恢复抗原受体交联引起的周期素依赖性激酶Cdk2活性的降低 ,以及Rb蛋白磷酸化水平的下降 ,并使细胞周期恢复运转。
短句来源
     In the experiment, the relationships of RB protein phosphorylation state and the results of the cell differentiation and cell cycle were according to the previous reports.
     实验中RB蛋白磷酸化状态与细胞分化和细胞周期关系与文献报道一致。
短句来源
  “rb蛋白磷酸化”译为未确定词的双语例句
     Objective: The multiple tumor suppressor gene P16 encode the P16 protein, which competitively binds to cyclin-dependent kinase 4 (CDK4) and inhibits its ability to interact with cyclinDl and phosphorylate the KB protein then to control the Gl/S check point of cell cycle as well.
     目的:多肿瘤抑制基因P16编码蛋白P16可竞争结合CDK4或CyclinD-CDK4复合物,阻止RB蛋白磷酸化,在细胞周期G1/S限制点起关键负调控作用,目前认为其失活机制主要有:纯合性缺失、点突变及启动子区DNA的5'CpG岛甲基化。
短句来源
     Overexpression of p16 INK4A in A549 cell line caused a G1 phase arrest with the inhibition of phosphorylation of Rb protein.
     p16 INK4A的表达能使细胞产生明显的G1期阻滞并伴随着Rb蛋白磷酸化状态的改变 ,Rb蛋白主要以低磷酸化形式存在。
短句来源
     Effect of sodium selenite on phosphorylation of retinoblastoma protein of human promyelocytic leukemia cells (HL-60)
     亚硒酸钠对人早幼粒白血病细胞的RB蛋白磷酸化的影响
短句来源
     Western blot confirmed EGCG effectively downregulated phosphor-Erk1/2 and phosphor-Rb prorein levels,while total Erkl/2 and Rb protein levels were not affected.
     免疫印迹结果显示:EGCG能下调Erk1/2蛋白的磷酸化水平,其作用与浓度和作用时间相关。 EGCG能下调Rb蛋白磷酸化水平,其调节作用与浓度有关。
短句来源
     Western blotting analysis showed that RA and sodium selenite influenced phosphorylation of retinoblasoma protein in HL-60 cells.
     Westernbloting结果显示:RA和硒可影响该细胞RB蛋白磷酸化与去磷酸化状态。
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  相似匹配句对
     PHOSPHORYLATION OF SOY PROTEIN
     大豆蛋白磷酸化
短句来源
     Western blot confi rmed the expression o f phosphorylated Rb protein significantly downregulated.
     免疫印迹检测磷酸化Rb蛋白表达下调。
短句来源
     The role of dephosphorylated RB protein in human breast cancer cell apoptosis
     去磷酸化RB蛋白在乳腺癌细胞凋亡中的作用
短句来源
     Relationship between cell apoptosis and dephosphorylated RB protein in human breast cancer
     人乳腺癌细胞凋亡与去磷酸化RB蛋白的关系
短句来源
     the expressive levels of dephosphorylated RB protein were detected with immunocytochemistry.
     采用免疫细胞化学法检测去磷酸化RB蛋白的表达水平。
短句来源
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  retinoblastoma protein phosphorylation
Revisiting retinoblastoma protein phosphorylation during the mammalian cell cycle
      
TRAIL-induced cell growth in resistant cells occurred through increased cell cycle progression as determined by flow cytometry and Western blot analysis of retinoblastoma protein phosphorylation.
      
Finally, the extent of retinoblastoma protein phosphorylation was assayed by Western blot in cells cultured with and without TAT-HA-p15.
      
In cyclin D1 null mice, E2 also induces retinoblastoma protein phosphorylation and DNA synthesis in a normal manner.
      
  rb protein phosphorylation
Fig 6. lmrnunoblot analysis of Rb protein phosphorylation after treatment RWLeu-4and with 1.25-VD3.
      
Rb protein phosphorylation allows cells to enter the S phase from G1.
      
The reduction in Cdk2 activity was determined by a reduction in Rb protein phosphorylation, which is a substrate of Cdk2/cyclin E complexes.
      


Analysis of Rb protein showed that the protein had a half time of more than 10 hours, and was synthesized at all phases of cell cycle. It could be phosphorylated. Regulation of phosphoryla non and quantity of Rb protein were cell-cycle-dependent. Newly synthesized Rb protein was underphosphorylated in cells at G, and G, phases, and was phosphorylated at multiple sites at G1/S boundary and in S phase. The underphosphorylated Rb protein may restrict the cell proliferation.

研究Rb基因产物的代谢动力学和功能调节,发现整个细胞周期中都有Rb蛋白合成,其含量随细胞周期进行而变化,蛋白代谢的半衰期约为11—12小时,有非磷酸化和多种程度磷酸化形式。Rb蛋白的磷酸化水平是随细胞周期过程和细胞生长状态而变化的,在G0、G1期蛋白处于低磷酸化状态,到达G1/S界限,细胞获得磷酸化Rb蛋白的能力.

Centrifugal elutriation method have been used to obtain a homogeneous cell population with regard to cell-cycle phases and stage of differentiation. In the presence of retinoic acid, the synchronous G0/G1 HL60 cells could completed first cell -cycle, the phosphorylation of Rb protein varied in the phases of cell-cycle. However the RA induced cells could not entry the second cell-cycle, but started to differentiate, and the Rb protein was observed to be in a state of under-level phosphorylation. The under level...

Centrifugal elutriation method have been used to obtain a homogeneous cell population with regard to cell-cycle phases and stage of differentiation. In the presence of retinoic acid, the synchronous G0/G1 HL60 cells could completed first cell -cycle, the phosphorylation of Rb protein varied in the phases of cell-cycle. However the RA induced cells could not entry the second cell-cycle, but started to differentiate, and the Rb protein was observed to be in a state of under-level phosphorylation. The under level or dephosphorylation of Rb protein might be attributed to the induction of cell differentiation by retinoic acid.

离心洗脱技术可分离到HL60细胞周期中同步的GO/G1期细胞.被视黄酸(RA)诱导的G0/G1细胞可以进行一个正常的细胞周期,Rb蛋白磷酸化水平随细胞周期而变化.但不能进入第二个细胞周期,细胞开始分化,Rb蛋白处于低磷酸化水平.Rb蛋白磷酸化水平的降低,是由于RA首先诱导细胞分化,使细胞生长停止,分化的细胞失去磷酸化蛋白能力的结果

D-typecyclinsbeingconsideredasoncogenespromoteprogressionofthecelthroughtheG1phaseofthecelcyclebyCDK4mediatedphosphorylationoftheretinoblastomaprotein.TheactivitiesofCDK4isconstrainedbyinhibitorssuchasp16,theproductoftheCDKN2intumorcelsandprimarytumorssuggeststhatp16actsasatumorsuppressor.Weexaminedtheseproteinsandgenesbyimmunohistochemistryandinsituhybridizationtechniquesin41primaryesophagealcancers.Overex-pressionofcyclinD1wasrevealedin26/41samples(63.4%)andalsointhemucosaadjacenttothecan-cersin10of26cyclinD1overexpressionsamples,whichalsohavehighlevelsofcyclinD1.P16wasunde-tectablein13of41samples.Interestingly,17of24Rbpositivecancershadnoorlowp16,while9Rb-negativecancersshowedhighlevelsofp16.TheseresultssuggestthattheoverexpressionofcyclinD1maybeacommonmolecularabnormalityandanearlymoleculareventinesophagealcancer,folowedei-therbyRbloss,asoccurredinRbnegativesamples,orbylossofp16,asoccurredinp16negativesam-ples.CyclinD1overexpressionandRbinactivationcancoexistinesophagealcancer.However,thereisareciprocitybetweenRbinactivationandp16expresioninesophagealcancer.Thus,abnormalityinthenegativefeedbackregulatorypathwayofcyclinD1/CDK4,Rbandp16maybeinvolvedinthemolecularmechanismofesophagealcancer....

D-typecyclinsbeingconsideredasoncogenespromoteprogressionofthecelthroughtheG1phaseofthecelcyclebyCDK4mediatedphosphorylationoftheretinoblastomaprotein.TheactivitiesofCDK4isconstrainedbyinhibitorssuchasp16,theproductoftheCDKN2intumorcelsandprimarytumorssuggeststhatp16actsasatumorsuppressor.Weexaminedtheseproteinsandgenesbyimmunohistochemistryandinsituhybridizationtechniquesin41primaryesophagealcancers.Overex-pressionofcyclinD1wasrevealedin26/41samples(63.4%)andalsointhemucosaadjacenttothecan-cersin10of26cyclinD1overexpressionsamples,whichalsohavehighlevelsofcyclinD1.P16wasunde-tectablein13of41samples.Interestingly,17of24Rbpositivecancershadnoorlowp16,while9Rb-negativecancersshowedhighlevelsofp16.TheseresultssuggestthattheoverexpressionofcyclinD1maybeacommonmolecularabnormalityandanearlymoleculareventinesophagealcancer,folowedei-therbyRbloss,asoccurredinRbnegativesamples,orbylossofp16,asoccurredinp16negativesam-ples.CyclinD1overexpressionandRbinactivationcancoexistinesophagealcancer.However,thereisareciprocitybetweenRbinactivationandp16expresioninesophagealcancer.Thus,abnormalityinthenegativefeedbackregulatorypathwayofcyclinD1/CDK4,Rbandp16maybeinvolvedinthemolecularmechanismofesophagealcancer.

细胞周期素D1促进G1期细胞进程是通过刺激细胞周期依赖激酶(CDKs)介导的Rb蛋白的磷酸化作用而实现。细胞周期素D1被认为是一种癌基因。CDK4的酶活性又受一些抑制蛋白如p16的限制,后者是存在于染色体9p21上的CDKN2基因的产物,在多种肿瘤细胞系和原发肿瘤中频发缺失和突变,被认为是抑癌基因。为了解它们在食管癌发生发展中作用,用免疫组织化学及原位杂交方法,在41例原发食管癌中检测了Rb、p16、细胞周期素D1的蛋白表达及部分肿瘤中细胞周期素D1和p16基因的存在状态。26/41例(63.4%)显示细胞周期素D1过度表达,10例在对应的癌旁增生上皮也显示细胞周期素D1的过度表达。13/41例p16表达阴性,4例呈弱阳性。24例Rb阳性的标本中,17例显示p16不表达或低水平表达,而9例Rb表达阴性的标本均显示p16表达增高。结果提示,在食管癌形成过程中,细胞周期素D1是一常见的分子异常,并且可能是一早期分子事件,随即而来的分子改变可以是Rb的失活或/和p16的失活;Rb的失活与细胞周期素D1激活在食管癌中可共同存在;Rb失活与p16表达之间存在负相关关系;食管癌的分子发病机制可能涉及CDK4/细胞周期素?

 
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