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retinoblastoma protein rb
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  相似匹配句对
     protein.
     protein。
短句来源
     Retinoblastoma binding protein 7;
     视网膜母细胞结合蛋白7;
短句来源
     Significance of PTEN protein expression of in retinoblastoma
     视网膜母细胞瘤组织中PTEN蛋白表达的意义
短句来源
     Expression of P~(53)gene protein in retinoblastoma
     视网膜母细胞瘤中P~(53)蛋白的免疫组化研究
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     Precise on protein
     精确蛋白质日粮
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  retinoblastoma protein rb
During HCMV infection, one of its proteins interacts with a cell growth regulatory protein, the retinoblastoma protein (Rb) and stimulates DNA synthesis which is associated with chromosomal damage and cellular mitotic arrest.
      
p53, p16/INK4a, p14/ARF, p15/INK4b, retinoblastoma protein (Rb), and Phosphatase and tensin homologue deleted from chromosome 10 (PTEN)) also participate actively in the development of the transformed phenotype.
      
The retinoblastoma protein (Rb) is one of a growing list of tumor suppressors.
      
No published data are available about the expression of peroxisome proliferator-activated receptor γ (PPARγ) and the role of PPARγ in retinoblastoma protein (RB)-deficient human colorectal cancer (CRC) cells (SNU-C4 and SNU-C2A).
      
The retinoblastoma protein Rb is part of a conserved pathway that controls the activation of cell division in animals.
      
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Purpose To study expression of the tumor suppressor gene retinoblastoma protein (Rb) before and after apoptosis of SHG?44 glioma cell. Methods Rb expression was detected in SHG?44 cells by Western blot using N terminal Rb monoclone antibody.And the change of Rb expression after apoptosis induced by VP16 was examined. Results A 70×10 3 with N terminal Rb was found in SHG?44 cell line.After cell apoptosis,Rb was cleaved into a 48×10 3 protein with...

Purpose To study expression of the tumor suppressor gene retinoblastoma protein (Rb) before and after apoptosis of SHG?44 glioma cell. Methods Rb expression was detected in SHG?44 cells by Western blot using N terminal Rb monoclone antibody.And the change of Rb expression after apoptosis induced by VP16 was examined. Results A 70×10 3 with N terminal Rb was found in SHG?44 cell line.After cell apoptosis,Rb was cleaved into a 48×10 3 protein with N?terminal and the glioma cells were arrested at G 11 phase. Conclusions A mutant Rb protein was expressed in SHG?44 cells.There is close relationship between Rb cleavage and apoptosis in glioma.

目的 研究抑癌基因Rb在人胶质瘤SHG 44细胞调亡前后的表达情况。方法 利用N端Rb蛋白单克隆抗体通过Western印迹法检测SHG 44胶质瘤细胞株Rb蛋白的表达情况 ,并观察用VP16诱导细胞凋亡后Rb蛋白表达的改变。结果 在SHG 44胶质瘤细胞株中存在一相对分子质量约 70× 10 3 、具有N端的Rb蛋白。细胞凋亡后 ,Rb蛋白有裂解现象 ,出现一具有N端的约 48× 10 3 的裂解蛋白 ,并使细胞停滞于G1期。结论 在胶质瘤SHG 44细胞中有Rb基因突变体的表达 ,Rb蛋白的裂解与细胞凋亡密切相关。

Objective To understand the experimentnl resluts and the advance in gene therapy for restenosis of the vessel. Method Literature review was made on gene therapy for restenosis directly at cytotoxic, cell cycle regulators, intracellular signal transducers, transcription factors, cytokines growth factors, nitric oxide and Fas ligand. Results cytotoxic gene therapy by thymidine kinase and cytosine deaminase, mutant retinoblastoma protein (Rb), cyclin-dependent kinases(cdk) inhibitors (such...

Objective To understand the experimentnl resluts and the advance in gene therapy for restenosis of the vessel. Method Literature review was made on gene therapy for restenosis directly at cytotoxic, cell cycle regulators, intracellular signal transducers, transcription factors, cytokines growth factors, nitric oxide and Fas ligand. Results cytotoxic gene therapy by thymidine kinase and cytosine deaminase, mutant retinoblastoma protein (Rb), cyclin-dependent kinases(cdk) inhibitors (such as p21 p27 and p53), antisense basic fibroblast growth factor (bFGF) blocking intracellular signal transduce by A-Raf and C-Raf, antisense Ag βγ, promoting NO, β-nterferon, vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), β chain synthesize suppressing nuclear factor-kB (NF-kB) overexpression of gax and Fas ligand can inhibit restenosis of the vessel. Conclusions The effect of gene therapy for restenosis of the vessed is obvious in experimental studies. Conbination of more gene and several links gene therapy is the research direction in the future.

目的 掌握基因治疗血管再狭窄的实验结果和发展方向。方法 针对细胞毒素基因、细胞周期调节因子、细胞因子和生长因子、细胞内信号感应器、一氧化氮、转录因子、Fas配体等作用或调节环节基因治疗实验研究文献 ,进行文献综述。结果 胸腺嘧啶核苷激酶 (HSV tk)和胞嘧啶脱氨酶细胞毒基因治疗、突变的Rb、cdk抑制因子p2 1,p2 7,p5 3 ,β 干扰素、血管内皮细胞生长因子 (VEGF )、反义碱性成纤维细胞生长因子 (bFGF)、血小板衍化生长因子 (PDGF) β ,A Raf和C Raf的反义寡核苷酸及AGβγ等阻断细胞内信号传递、增加NO的合成、抑制平滑肌细胞 (SMC )的细胞核因子kB(nuclearfactor kBNF kB )、促进gax和Fas配体表达等基因治疗可明显抑制血管再狭窄。结论 基因治疗再狭窄治疗实验疗效明显 ,多基因多环节的联合基因治疗是今后的研究方向

Necdin is only expressed in postmitotic neurons, suggesting that necdin has a function to keep differentiated neurons staying in the postmitotic state. Necdin is a growth suppressor and binds to SV40 large T antigen, adenovirus E1A, transcription factor E2F1 and tumor suppress gene p53, which is similar to another known growth suppressor retinoblastoma protein Rb. The necdin gene is localized to chromosome 15q11.2 q12 within the Prader Willi syndrome deletion region, and may contribute to some symptoms...

Necdin is only expressed in postmitotic neurons, suggesting that necdin has a function to keep differentiated neurons staying in the postmitotic state. Necdin is a growth suppressor and binds to SV40 large T antigen, adenovirus E1A, transcription factor E2F1 and tumor suppress gene p53, which is similar to another known growth suppressor retinoblastoma protein Rb. The necdin gene is localized to chromosome 15q11.2 q12 within the Prader Willi syndrome deletion region, and may contribute to some symptoms of PWS. Here the necdin gene and protein, its biological functions and contributions to genetic disease are briefly reviewed. [

在神经系统 ,Necdin只在成熟神经元的细胞核中表达 ,可能与成熟神经元分裂静止状态的保持有关。近年的研究表明 ,Necdin是一种生长抑制蛋白 ,能与多种因子如SV4 0大T抗原 ,腺病毒E1A ,转录因子E2F1以及肿瘤抑制蛋白p5 3等结合 ,在功能上类似于成视网膜瘤蛋白Rb。necdin基因缺陷时 ,会引起脑内 ,特别是下丘脑神经元分化障碍。人类necdin基因位于PWS综合征的基因缺失区 ,可能与PWS的一些症状有关。本文从Necdin蛋白的基本概况 ,生物功能以及Necdin与疾病三个方面进行了综述

 
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