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rb途径
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  rb pathway
     Conclusion The methylation of p16 INK4a or RB is related with the tumorigenesis and progression of atypical and anaplastic meningiomas, and a probable mechanism is that methylation causes the loss of expression and leads to dysfuncation of the p16 INK4a /cyclin D1/CDK4/RB pathway.
     结论 p16 INK4 a或 RB的甲基化与不典型和间变性脑膜瘤的发生发展有关 ,其机制可能是甲基化使蛋白表达丢失并导致 p16 INK4 a/细胞周期蛋白 D1/ CDK4 /RB途径功能障碍
短句来源
     The inhibition of cell growth by p16 on HCC cells could be dependent on intact RB pathway.
     而 p16 INK4 A对肝癌细胞生长抑制的作用可能依赖于 RB途径的完整性。
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  “rb途径”译为未确定词的双语例句
     Recent studies have found that p16 and p21, the specific suppressors of cyclin/CDK4/6, can regulate the phosphorylation of pRb and control the cell cycle progression through p16 - cyclm/CDK - Rb and p53 - p21 - cyclin/CDK - Rb pathway.
     近年来的研究发现,许多基因通过信号传导途径调节pRb发生细胞周期依赖性磷酸化。 其中被广泛研究的是p16-cyclin/CDK-Rb途径和p53-p21-cyclin/CDK-Rb途径
短句来源
     The Rb abnormality was observed in 20% of malignant tumors, and the disruptions of p16 - cyclin/CDK - Rb or p53 - p21 -cyclin/CDK - Rb pathway were in 80%.
     关于Rb基因家族及其传导途径异常与肿瘤的关系,许多研究证明,约20%的恶性肿瘤存在Rb异常,80%的肿瘤存在p16-cyclin/CDK-Rb途径或p53-p21-cyclin/CDK-Rb途径中某一环节的异常。
短句来源
     Our results found that Epstein-Barr virus inhibited the expression of p16INK4a, at the same time, E2F1 expression were strongly increased in EBV-infected cells, however, as for the expression of p53 and p21WAF1/CIP1, there was no difference between EBV-infected cells and non-infected cells.
     结果表明,EB病毒通过抑制p16~(INK4a)表达而阻断p16~(INK4a)/Rb途径,上调转录因子E2F1,而对p53、p21~(WAF1/CIP1)表达无明显的影响。
短句来源
     The P16-cyclin Dl-Rb pathway plays important role in Gl phase regulation. P16 functional defects, Cyclin Dl overexpression or Rb alteration will disrupt the balance of cell cycle regulation and promote carcinogenesis.
     P16-Cyclin D1-Rb途径在G_1期调控中起关键作用,P16的功能缺陷、Cyclin D1的过表达或Rb的突变或缺失都将破坏这一途径和细胞周期调控的稳态平衡,导致肿瘤的发生。
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  相似匹配句对
     transport route;
     转运途径;
短句来源
     Deregulation Significance of Rb Tumor Suppression Pathway during Carcinogenesis of Lung Cancer in Wistar Rats
     大鼠肺癌癌变过程中Rb肿瘤抑制途径失控的意义
短句来源
     THE ENERGY SAVING APPROACHES OF COKE OVENS
     炼焦炉的节能途径
短句来源
     Nuclear envelope dystrophies show a transcriptional fingerprint suggesting disruption of Rb-MyoD pathways in muscle regeneration
     核膜营养不良显示促成肌肉再生Rb-MyoD途径破裂的转录指纹
短句来源
     Discussion for RB functions
     RB功能探讨
短句来源
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  rb pathway
This was mediated by the Rb pathway, as shown by an E2F1-driven reporter assay and Western immunoblot of phosphorylated Rb protein.
      
These results suggested that deregulation of p16-cyclin D1/Cdk4-Rb pathway, but not oncogenic activation of ras, plays a crucial role in bladder tumorigenesis induced by bladder calculi.
      
We analyzed the inactivation of the INK4 family CKI/CDK/RB pathway by gene promoter hypermethylation in leukemogenesis.
      
Therefore, methylation inactivation of the INK4/CDK/RB pathway in leukemia involved primarily p15 and occasionally p16, but not p18 or RB.
      
Overall, alterations of the p53/MDM2/Rb pathway occurred in 30 of 45 liposarcomas (66.6%).
      
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Cell cycle deregulation is regarded as an important event to involve in cellular immortalization. To confirm the role of cell cycle deregulation in human fetal nasopharyngeal epithelial cells escaping from the replicative senescence induced by Epstein-Barr virus infection, we detected expression of cell cycle regulators, such as p16INK4a, p21WAF1/CIP1, p53, and E2F1 with Western blotting and im-munocytochemisty in this study. Our results found that Epstein-Barr virus inhibited the expression of p16INK4a, at...

Cell cycle deregulation is regarded as an important event to involve in cellular immortalization. To confirm the role of cell cycle deregulation in human fetal nasopharyngeal epithelial cells escaping from the replicative senescence induced by Epstein-Barr virus infection, we detected expression of cell cycle regulators, such as p16INK4a, p21WAF1/CIP1, p53, and E2F1 with Western blotting and im-munocytochemisty in this study. Our results found that Epstein-Barr virus inhibited the expression of p16INK4a, at the same time, E2F1 expression were strongly increased in EBV-infected cells, however, as for the expression of p53 and p21WAF1/CIP1, there was no difference between EBV-infected cells and non-infected cells. The results show that EBV inactivates p16INK4a/pRB pathway and then induces E2F1 activity and it is implicated that Epstein-Barr virus-medicated cell cycle deregulation plays an important role in the immortalization of human nasopharyngeal epithelial cells. These data will be helpful for further studying the carcinogenesis of nasopharyngeal carcinoma.

细胞周期调控紊乱是细胞永生化进程中一个重要的分子事件,本文利用Western blotting和S-P法分别检测p16~(INK4a)、p53、p21~(WAF1/CIP1)和E2F1的蛋白表达,试图从细胞周期调控的角度,探讨EB病毒诱导人胎鼻咽上皮细胞逃避老化期的分子机制。结果表明,EB病毒通过抑制p16~(INK4a)表达而阻断p16~(INK4a)/Rb途径,上调转录因子E2F1,而对p53、p21~(WAF1/CIP1)表达无明显的影响。结果初步揭示,EB病毒介导的p16~(INK4a)/Rb/E2F1细胞周期调控紊乱参与了人胎鼻咽上皮细胞逃避老化期过程,为进一步探讨鼻咽癌发病机制提供了科学依据。

Objective Both tumor suppressor p16INK4A and p15INK4B are members of INK family of CDK inhibitor. Although the role of p16 has been well documented, the role of p15 and its signaling pathway remain less well studied. This study was aimed to assess the effect of p16 and p15 on hepatocarcinoma cell lines with different status of Rb gene. Methods After identification of the genetic status of p16, p15 as well as Rb of human hepatocellular carcinoma (HCC) cell lines BEL7402, SMMC7721 with the use of multiple PCR,...

Objective Both tumor suppressor p16INK4A and p15INK4B are members of INK family of CDK inhibitor. Although the role of p16 has been well documented, the role of p15 and its signaling pathway remain less well studied. This study was aimed to assess the effect of p16 and p15 on hepatocarcinoma cell lines with different status of Rb gene. Methods After identification of the genetic status of p16, p15 as well as Rb of human hepatocellular carcinoma (HCC) cell lines BEL7402, SMMC7721 with the use of multiple PCR, the eukaryotic expression p16 and p15 recombinants pXJ-p16 and pXJ-p15 were constructed, respectively. The existence of exogenous p16, p15 genes, and the expression of p16 and p15 were assayed by means of PCR and RNA dot blotting. Finally, the proliferation and apoptosis were studied by using MTT, colony formation assay and flow cytometry. Results Neither deletion of p16 nor p15 was detected in the two cell lines. However, Rb exons 14-16 instead of exons 22-23 deletion existed in SMMC7721. The increased mRNA expression level of p16 was found in BEL7402-p16 and SMMC7721-p16, while increased mRNA expression level of p15 was found in BEL7402-p15. The endogenous p16 and p15 genes were transcripted at low level. The cell growth and colony formation were decreased in BEL7402-p15, compared with either mock cell BEL7402 or vector control cell BEL7402-pXJ. Also shown in this study were an altered G1 phase population from 37.7% to 43.6%, an S phase population from 22% to 13% (P<0.05), and a Sub G1 peak (apoptosis peak) in BEL7402-p15. Conversely, BEL7402-p16 with endogenous p16 gene showed neither difference in cell cycle population nor difference in colony formation rate, compared with control cell groups. Additionally,SMMC7721-p16 cell growth was not inhibited by exogenous p16 gene. Conclusion p15 significantly arrested cell proliferation and induced apoptosis in BEL7402 in vitro, and the function was not influenced by endogenous p15 gene. The inhibition of cell growth by p16 on HCC cells could be dependent on intact RB pathway.

目的 为探讨抑癌基因 p16 INK4 A和 p15 INK4 B对 Rb基因状态不同的人肝癌细胞系增殖和凋亡的影响。方法 在分析细胞系遗传背景鉴定基础上采用脂质体将构建的 p XJ- p16、p XJ- p15重组质粒转染人肝癌细胞系 BEL74 0 2 (p16 +/ p15 +Rb+)和 SMMC772 1(p16 +/ p15 +/ Rb- )。应用 PCR、RNA斑点印迹、MTT、集落形成、流式细胞仪等技术检测外源性 p16和 p15基因、m RNA表达及其对肝癌细胞增殖、凋亡的影响。结果 经转染的 BEL74 0 2 - p16 ,BEL74 0 2 - p15细胞 ,分别存在外源性 p16、p15基因 ,在含外源基因细胞中相应的 m RNA表达增强 ;BEL74 0 2 - p15细胞生长速度、集落形成率显著低于对照细胞 BEL 74 0 2 (P<0 .0 1) ;细胞周期分析观察到与亲本细胞比较 ,BEL 74 0 2 - p15的 G1期细胞由 37.7%增高到 4 3.6 % ,S期细胞由 2 2 %下降到 13% (P<0 .0 5 ) ,并出现 G1亚峰 (凋亡峰 )。与此相反 ,B...

目的 为探讨抑癌基因 p16 INK4 A和 p15 INK4 B对 Rb基因状态不同的人肝癌细胞系增殖和凋亡的影响。方法 在分析细胞系遗传背景鉴定基础上采用脂质体将构建的 p XJ- p16、p XJ- p15重组质粒转染人肝癌细胞系 BEL74 0 2 (p16 +/ p15 +Rb+)和 SMMC772 1(p16 +/ p15 +/ Rb- )。应用 PCR、RNA斑点印迹、MTT、集落形成、流式细胞仪等技术检测外源性 p16和 p15基因、m RNA表达及其对肝癌细胞增殖、凋亡的影响。结果 经转染的 BEL74 0 2 - p16 ,BEL74 0 2 - p15细胞 ,分别存在外源性 p16、p15基因 ,在含外源基因细胞中相应的 m RNA表达增强 ;BEL74 0 2 - p15细胞生长速度、集落形成率显著低于对照细胞 BEL 74 0 2 (P<0 .0 1) ;细胞周期分析观察到与亲本细胞比较 ,BEL 74 0 2 - p15的 G1期细胞由 37.7%增高到 4 3.6 % ,S期细胞由 2 2 %下降到 13% (P<0 .0 5 ) ,并出现 G1亚峰 (凋亡峰 )。与此相反 ,BEL74 0 2 - p16细胞增殖未见抑制 ,细胞周期分布无明显差异 ,集落形成率也未见减少。此外 ,SMMC772 1- p16细胞增殖也无抑制。结论 外源性 p15 INK4 B具有抑制人肝癌细胞生长 ,诱导细胞凋亡的作用 ,其作用不受内源性p15影响。而 p16 INK4 A对肝癌细胞生长抑制的作用可能依赖于 RB途径的完整性。

Objective To investigate the methylation of p16 INK4a and RB gene, and the expression of p16 INK4a in meningiomas. Methods Methylation-specific polymerase chain reaction (MSP) was used to detect the methylation of p16 INK4a and RB in 50 cases of meningiomas, and immunostaining was performed to analyze the protein expression of p16 INK4a in 25 of those cases. Results No methylation was found in the benign meningiomas, whereas methylation of p16 INK4a or RB occurred...

Objective To investigate the methylation of p16 INK4a and RB gene, and the expression of p16 INK4a in meningiomas. Methods Methylation-specific polymerase chain reaction (MSP) was used to detect the methylation of p16 INK4a and RB in 50 cases of meningiomas, and immunostaining was performed to analyze the protein expression of p16 INK4a in 25 of those cases. Results No methylation was found in the benign meningiomas, whereas methylation of p16 INK4a or RB occurred in 6(37.5%) cases of grade Ⅱ tumors and 4(28 6%) cases of grade Ⅲ tumors, and among these cases, an atypical meningioma showed methylation of both genes. Thirteen cases showed p16 INK4a positive expression, but none of them was methylated. Conclusion The methylation of p16 INK4a or RB is related with the tumorigenesis and progression of atypical and anaplastic meningiomas, and a probable mechanism is that methylation causes the loss of expression and leads to dysfuncation of the p16 INK4a /cyclin D1/CDK4/RB pathway.

目的 检测脑膜瘤中发生 p16 INK4 a和 RB基因甲基化的情况及对蛋白表达的影响。方法 用甲基化特异性聚合酶链反应对 5 0例脑膜瘤进行了 p16 INK4 a和 RB的甲基化分析 ;并对其中的 2 5例检测了p16 INK4 a蛋白的表达。结果 良性脑膜瘤中没有检测到甲基化 ,分别有 6例 级 ( 37.5 % )和 4例 级( 2 8.6 % )肿瘤发生至少一种基因的甲基化 ,其中有 1例不典型脑膜瘤同时发生了两种基因的甲基化。全部13例 p16 INK4 a阳性表达的肿瘤都是没有检测到甲基化者。结论 p16 INK4 a或 RB的甲基化与不典型和间变性脑膜瘤的发生发展有关 ,其机制可能是甲基化使蛋白表达丢失并导致 p16 INK4 a/细胞周期蛋白 D1/ CDK4 /RB途径功能障碍

 
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