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rb蛋白的磷酸化
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  rb phosphorylation
     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 .
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  “rb蛋白的磷酸化”译为未确定词的双语例句
     Cdk2 activity was detected by in vitro kinase assay and phosphorylation of Rb protein was monitored by Western blot.
     用体外激酶实验检测Cdk2的活性 ,Westernblot检测Rb蛋白的磷酸化水平。
短句来源
     The insect expressing vectors could express Cyclin D1 and CDK4 proteins which possessed ability of phosphorylating Rb protein, showing biological activity.
     研究表明 ,昆虫细胞表达的细胞周期蛋白D1和CDK4蛋白能促进Rb蛋白的磷酸化 ,具有生物活性 .
短句来源
     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.
     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.
短句来源
     As a result,Rb protein could be regulated in its phosphorylation state by ATRA. Furthermore expression of c myc was suppressed by ATRA.
     另外 ,ATRA可以调节 Rb蛋白的磷酸化和 c- myc蛋白的表达 .
短句来源
     In many aging cell lines, the activity of retinoblastoma (Rb) gene is increased . It coidifies for a protein involved in the regulation of cell cycle and cell proliferation and it plays an important role of signaling pathways involved in cellular senescence.
     在多种衰老细胞系中,抑癌基因Rb的活性增加,其编码的Rb蛋白参与细胞周期的调控,调节细胞增值,在细胞衰老信号传递中扮演重要角色,其中Rb蛋白的磷酸化状态与细胞增值分裂密切相关。
短句来源
  相似匹配句对
     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
     PHOSPHORYLATION OF SOY PROTEIN
     大豆蛋白磷酸化
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蛋白表达水平。
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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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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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