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transcriptional相关的网络例句

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与 transcriptional 相关的网络例句 [注:此内容来源于网络,仅供参考]

The characteristical time-dependent expression of transcriptional factors HNF4α, C/EBPα, and C/EBPβ during the hepatocyte differentiation by bone marrow stem cells demonstrates that the expressions of these transcriptional factors are closely related to the initiation and maintenance of hepatocyte differentiation.

结论在肝细胞分化过程中,转录因子HNF4α、C/EBPα和C/EBPβ呈特征性时序表达,表明骨髓间充质干细胞在向肝细胞分化时,肝细胞相关转录因子的表达与细胞分化的启动和维持密切相关。

PIAS proteins play roles mainly through two mechanisms: acting as SUMO E3 ligases to promote modifications of some transcriptional factors and cofactors, especially sumoylation, and to regulate their transcriptional activation; acting as structural proteins to offer platforms for protein-protein interactions and to promote the abstraction and recruitment of other regulators in the cellular signal pathway complexes or gene transcriptional complexes, companied by the subnuclear location of target proteins.

PIAS蛋白的调控机制主要有两种:一种是通过其自身所具有的SUMO(small ubiquitin-related modifiers)E3连接酶活性,促进对一些转录因子、转录辅因子的化学修饰,尤其是SUMO化修饰,从而调控它们的转录活性;另一种是作为构架蛋白,为蛋白质之间的相互作用提供平台,促进细胞信号通路复合物或基因转录复合物中其它调节蛋白的去除和募集,并涉及到靶蛋白的亚核定位。

The stable clones are further identified by RT-PCR and Western blot; 6 MTT assay is used to investigate the effect of ZNRD1 on the cell growth of cells (AGS, SGC7901, MKN28, NIH3T3, GES-1); 7 Soft agar assay is used to investigate the effect of ZNRD1 on the clonality of cells (AGS, MKN28); 8 Nude mice assay is used to investigate the effect of ZNRD1 on the cell growth of gastric cancer cells (AGS, MKN28); 9 Flow cytometry is used to investigate the effect of ZNRD1 on the cell cycle distribution of cells (AGS, MKN28, NIH3T3, GES-1); 10 Flow cytometry is used to investigate the effect of ZNRD1 on the cell apoptosis of cells (AGS, MKN28, NIH3T3); 11 MTT assay is used to investigate the effect of ZNRD1 on the drug sensitivity of cancer cells (SGC7901, SGC7901/VCR, HL-60, HL-60/VCR) in vitro; 12 SRCA is used to investigate the effect of ZNRD1 on the drug sensitivity of gastric cancer cells (SGC7901, SGC7901/VCR) in vivo; 13 Flow cytometry is used to investigate the effect of ZNRD1 on adriamycin accumulation of cancer cells (SGC7901, SGC7901/VCR, HL-60, HL-60/VCR); 14 Transmission electron microscope is used to investigate the effect of ZNRD1 on the sensitivity of SGC7901 cells towards drug-induced apoptosis; 15 Flow cytometry and DNA ladder assay are used to investigate the effect of ZNRD1 on the sensitivity of cells (SGC7901, SGC7901/VCR, HL-60/VCR) towards drug-induced apoptosis; 16 Microarray is used to investigate the profiling of ZNRD1-responsive genes in gastric cancer cells (AGS, MKN28, SGC7901, SGC7901/VCR); 17 RT-PCR and Western blot are used to identify the results of microarray; 18 Reporter gene assay is used to investigate the effect of ZNRD1 on the transcriptional activity of cyclin D1; 19 Reporter gene assay is used to investigate the effect of ZNRD1 on the transcriptional activity of MDR1; 20 Kinase assay is used to investigate the effect of ZNRD1 on the activity of cyclin E-CDK2 kinase; 21 The antisensenucleic acids of p21 is used to inhibit the expression of p21, and flow cytometry is used to investigate the effect of p21 on ZNRD1-induced cell cycle arrest in gastric cancer cells; 22 The antisensenucleic acids of p27 is used to inhibit the expression of p27, and flow cytometry is used to investigate the effect of p27 on ZNRD1-induced cell cycle arrest in gastric cancer cells; 23 Liposome is used to up-regulate the expression of Skp2, and flow cytometry is used to investigate the effect of Skp2 on ZNRD1-induced cell cycle arrest in gastric cancer cells; 24 Western blot is used to investigate the effect of ZNRD1 on the stability of Skp2 and p27 in gastric cancer cells; 25 MVD assay is used to investigate the effect of ZNRD1 on the angiopoietic activity of gastric cancer cells; 26 ELISA is used to investigate the effect of ZNRD1 on the expression of VEGF165 in gastric cancer cells; 27 The roles of DARPP-32 in MDR of gastric cancer cells are investigated using gene transfection, MTT assay, SRCA, flow cytometry and DNA ladder assay.

应用杂交瘤技术制备ZNRD1的首个单克隆抗体;2)利用RT-PCR、Western blot和免疫组化检测ZNRD1在胃癌组织、胃炎组织、正常胃上皮组织、胃癌细胞和正常胃组织上皮细胞中的表达;3)构建ZNRD1的小干扰RNA载体,并测序鉴定;4)利用脂质体将ZNRD1的真核表达载体及其空载体转染胃癌细胞(AGS、SGC7901、MKN28)和小鼠成纤维细胞(NIH3T3),G418筛选后进行鉴定;5)利用脂质体将ZNRD1的小干扰RNA载体及其空载体转染药敏胃癌细胞(SGC7901)、正常胃组织上皮细胞(GES-1)、对长春新碱耐药的胃癌细胞(SGC7901/VCR)、药敏白血病细胞(HL-60)、对长春新碱耐药的白血病细胞(HL-60/VCR),G418筛选后进行鉴定;6)利用MTT实验检测ZNRD1高/低表达对细胞(AGS、SGC7901、MKN28、NIH3T3、GES-1)生长的影响;7)通过软琼脂克隆形成实验检测上调ZNRD1对AGS、MKN28细胞克隆形成能力的影响;8)通过裸鼠成瘤实验检测上调ZNRD1对AGS、MKN28细胞体内成瘤性的影响;9)通过流式细胞仪分析ZNRD1高/低表达对细胞(AGS、MKN28、NIH3T3、GES-1)的细胞周期的影响;10)通过流式细胞仪分析上调ZNRD1对细胞(AGS、MKN28、NIH3T3)的凋亡的影响;11)通过MTT实验检测ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR、HL-60、HL-60/VCR)体外药物敏感性的影响;12)通过肾包膜下移植法检测ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR)体内药物敏感性的影响;13)通过流式细胞仪分析ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR、HL-60、HL-60/VCR)内阿霉素蓄积和泵出的影响;14)通过透射电镜检测上调ZNRD1对SGC7901细胞凋亡敏感性的影响;15)通过流式细胞仪和DNA梯度试验检测ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR、HL-60)凋亡敏感性的影响;16)通过基因芯片检测ZNRD1高/低表达对胃癌细胞内基因表达谱的影响;17)利用RT-PCR、Western blot对基因芯片的结果进行鉴定;18)利用报告基因实验检测ZNRD1对cyclin D1的启动子活性的调节作用;19)利用报告基因实验检测ZNRD1高/低表达对MDR1的启动子活性的调节作用;20)利用激酶试验检测ZNRD1对cyclin E-CDK2 激酶活力的影响;21)利用反义核酸技术抑制p21的表达;通过流式细胞仪检测抑制p21对ZNRD1介导的细胞周期阻滞的影响;22)利用反义核酸技术抑制p27的表达;通过流式细胞仪检测抑制p27对ZNRD1介导的细胞周期阻滞的影响;23)利用脂质体转染法上调Skp2的表达;通过流式细胞仪检测上调Skp2对ZNRD1介导的细胞周期阻滞的影响;24)利用Western blot检测ZNRD1对p27和Skp2的蛋白稳定性的影响;25)利用微血管密度实验检测ZNRD1对AGS、MKN28细胞裸鼠移植瘤微血管形成的影响;26)利用ELISA检测ZNRD1对AGS、MKN28细胞培养上清和移植瘤匀浆中VEGF165含量的影响;27)利用脂质体转染法、MTT实验、肾包膜下移植法、流式细胞仪和DNA梯度试验检测新耐药相关分子DARPP-32对细胞(SGC7901、SGC7901/VCR、对阿霉素耐药的胃癌细胞SGC7901/ADR)多药耐药表型的影响;利用脂质体转染法和MTT实验检测下调ZNRD1对DARPP-32介导的胃癌多药耐药的调控作用。

While AcMNPV and BmNPV had no stimulatory effect in nonsensitive cell lines BmNPV hr3 has been demonstrated to increase the transcriptional activity of cislinked hel510 promoter. In this study, Sf-21, Bm-N and Hi-5 cell lines were transfected with pBmhel510luc-hr3down, and then were infected with each of AcMNPV, BmNPV and HyNPV. The results indicated that viral factors could interact with hr3 to significantly copromote the transcriptional level of hel510 promoter.

BmNPV hr3已被证明具有增强子功能,将hr3与hel510启动子顺式连接的质粒pBmhel510luc-hr3down转染Sf-21、Bm-N和Hi-5细胞后,再用上述三种病毒分别感染每一种细胞,hel510启动子的转录活性得到显著提高,表明病毒因子能够识别hr3,二者通过相互作用,共同增强解旋酶基因启动子的转录水平。

The transcriptional regulation of APP gene in neuronal cells may be important both as a model system for the analysis of transcriptional regulation of eukaryotic gene in neuron and playing the putatively central role of APP in the pathogenesis of the AD.

研究APP基因的转录调节,不仅可为真核基因在神经元中的表达调控提供一种模式,而且还可以进一步探讨其在AD病理学机制中的作用。

Transcriptional activity of ACL recombinants normalized by Renilla was significant difference with pGL3-Basic expect for construct -27 and -15 (P<0.01). Construct -919 contains highest activity. 3 times reduction of transcriptional activity from-919 to -679bp indicated that negative regulation factors located probably in this region. The activity started on construct -73 suggested the basal promoter activity was located within the -73 to +77bp region; Transcriptional activity of IDHβrecombinants was not significantly different between the recombinant -58 and pGL3-Basic. The activity started on construct -82, decreasing with the length of the fragment up to -164 in despite of a bit of fluctuation, and kept increasing from construct -164 up to -279. Thus, the basal promoter activity was located within the -82 to +16bp region, whereas the upstream 197bp conferred maximal transcriptional activity.

采用5'端缺失策略,结合启动子预测结果,分别构建了8个ACL基因和19个IDH3β基因启动子区重组子,将其转染猪PK15细胞系,并利用荧光素酶双报告基因系统检测了它们的活性,结果表明:在所构建的猪ACL基因5侧翼序列的8个重组子中,除pGL-ACL27和pGL-ACL15外,其它重组子的荧光素酶活性与阴性对照均达到极显著水平(P<0.01),表明它们均具有启动子活性,pGL-ACL919活性最强,到pGL-ACL679活性下降了将近3倍,说明从-919bp到-679bp区域可能存在负的调控位点,从pGL-ACL621到pGL-ACL73活性有小幅度下降,到pGL-ACL27活性降到与阴性对照水平无显著差异,表明维持该启动子的基本活性区域位于-73bp到+77bp之间;IDH3β基因启动子活性开始于pGL-IB82,然后虽然有些波动,但是活性一直下降直到-164bp处,之后活性又开始升高,直到-279bp处活性达到最高,这些表明维持该启动子的基本活性区域位于-82bp到+16bp之间,从-82到-279之间的179bp区域具有最高的启动子活性。

The Results displayed: DChanges of histological morphology in treating group is superior to the other two groups.(2Expression of BMP-2 at fracture region in treating group is obviously supeior to the other two groups(p.05) and advancely reach peak valuce at first weak.(3) transcriptional level of BMP-2 mRNA in treating group is obviously supeior to the other two groups(p.05) and samely advancely reach peak valuce at first weak.(4)In every period of fracture healing, the expression of BMP-2 and transcriptional level of BMP-2 mRNA appear dynamic change and begin to go up after fracture, moreover reached to peak value in two weaks, then go down gradually.

结果发现:(1)治疗组组织形态学检查明显优于其它二组;(2)治疗组骨折部位骨形态发生蛋白-2(BMP-2)的表达水平比其它二组明显提高(P<0.05),并在一周时提前达到高峰;(3)治疗组骨折部位骨形态发生蛋白-2(BMP-2)mRNA的转录水平比其它二组明显提高(P<0.05),同样在一周时提前达到高峰;(4)在骨折愈合的不同时期,BMP-2的表达及其mRNA的转录水平呈动态变化,即骨折后开始升高,2周左右达到高峰,以后逐渐下降。

Northern blot analysis of iNOS expression and iNOS stability revealed that bismuth subgallate (100 μM) significantly reduced the amount of iNOS mRNA and increased iNOS mRNA degradation. Because expression of iNOS is mediated by transcription factor, NF-κB, in the transcriptional level and immunosuppressor, TGF-β, at the post-transcriptional level, we examined the effect of bismuth subgallate on TGF-β1 production and NF-κB activity.

在本实验中,我们发现仅bismuth subgallate会减少以interferon-γ and lipopolysaccharide活化之RAW 264.7 巨噬细胞株中一氧化氮之含量,我们进一步以北方墨点分析iNOS mRNA含量及iNOS mRNA稳定性,结果显示处理bismuth subgallate的活化巨噬细胞中,iNOS mRNA含量较未处理之细胞明显地减少约60%,其iNOS mRNA半衰期较未处理之细胞明显地减少约50%。

P/CAF and p300 synergically increase the transcriptional activity of WT1 gene, their HAT domains are important in the course of WT1 gene transcriptional activation.

P/CAF和p300能够协同提高WT1基因的转录活性,在此过程中,P/CAF和p300的HAT区发挥重要作用。

NodD binds to and bends target promoters through anchoring two tandem and individual specific DNA sites. NodD functions as a tetramer, which has a V-shaped main body. Tetrameric NodD is to change its own conformation rather than its oligomeric forms in response to small signal molecules. The specific interaction between each NodD DNA-binding domain and each specific DNA site does not alter itself in spite of naringenin induction, and the induced conformational change is transferred from protein to DNA. Only the DNA conformation incited by induced NodD is competent for RNA polymerase to form the transcriptional open complex. It cannot be excluded that NodD may have protein-to-protein contacts with RNA polymerase, and that the NodD conformational change may also directly contribute to the transcriptional open complex formation. However, the NodD conformational change itself cannot serve as the determinant of the transcriptional molecular switch.

通过研究,我们提出了初步的NodD操纵子激活模型:第一,四聚体是NodD蛋白的功能单位,它通过铆钉两个串联的相对独立的DNA靶位点结合被诱导的启动子;第二,小分子配基的结合是改变NodD四聚体的构象而不是引发不同形式的寡聚体,在我们的模型中,NodD四聚体缩小其V形主体的弯折角,进而缩短其DNA结合功能域的间距;第三,小分子信号的诱导并没有改变NodD的DNA结合域和其DNA靶位点的相互作用,NodD的构象改变由蛋白质经其双铆钉位点传递给DNA;第四,只有诱导状态的NodD激发的DNA构象才能有效地使RNA聚合酶形成转录开放复合物;第五,不排除NodD与RNA聚合酶可能有直接的相互接触位点,不排除NodD构象的改变可能直接有利于RNA聚合酶形成转录开放复合物,但是我们认为NodD构象改变本身不是充当转录激活开关的决定因素。

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