查询词典 erk

To produce the scientific evidence for developing and manufacturing new antitumor drugs.Methods: 1 The inhibitory effect on cell growth of Hela was measured by MTT assay in treated or untreated groups (3.125, 6.25, 12.5, 25, 50μg/ml TAM and control) for three different treatment times (24h, 48h and 72h).2 Apoptosis and cell cycle were measured by FCM in four experimental groups (0, 4, 16, 40μg/ml TAM) for 48h.3 Adopting Wright and Giemse's staining to observe the morphology of Hela cells which treated with 40μg/ml TAM.4 Using invasion experiment to detect the Hela cells'invasive abilities which treated with 40μg/ml TAM.5 The protein expressional levels of P-ERK, ERK, C-myc and Cyclin D1 in Hela cells untreated or treated with 4, 16, 40μg/ml TAM for 24h were measured by Western blot.6 Expression of anti-apoptotic gene bcl-2, apoptotic gene bax and MMP-9 in Hela cells of four experimental groups (0, 4, 16, 40μg/ml TAM for 24h), were observed by revers transcription PCR.7 The protein expression of P-ERK, ERK, Bcl-2 and Bax in Hela cells treated with 40μg/ml TAM for 24h observed by laser scanning microscopes.

1采用四甲基偶氮唑蓝法检测不同浓度北豆根总碱(3.125、6.25、12.5、25、50μg/ml)处理不同时间(24、48和72小时)对Hela细胞增殖反应的抑制作用。2采用流式细胞技术(flow cytometry，FCM)检测不同浓度北豆根总碱(0、4、16、40μg/ml)作用48小时，对Hela细胞凋亡及周期变化的影响。3瑞氏-姬姆萨染色后显微镜观察北豆根总碱(0、40μg/ml)作用24小时后Hela细胞形态学变化。4采用Transwell小室法检测北豆根总碱(0、40μg/ml)作用24小时后对Hela细胞侵袭性的影响。5采用免疫印迹方法检测不同浓度北豆根总碱(0、4、16、40μg/ml)作用24小时后，Hela细胞中磷酸化ERK、ERK、C-myc、CyclinD1的表达变化。6采用逆转录-聚合酶链反应(revers transcription PCR，RT-PCR)半定量检测北豆根总碱(0、4、16、40μg/ml)作用24小时，Hela细胞抗凋亡基因bcl-2、促凋亡基因bax、基质金属蛋白酶-9(MMP-9)的表达变化。7应用激光共聚焦显微镜(laser scanning microscope，LSM)观察北豆根总碱(0、40μg/ml)作用24小时后，Hela细胞内P-ERK、ERK、Bcl-2、Bax蛋白的表达变化。

The results showed that the inhibition of the ERK pathway in dHP resulted in anhedonia and anxiety-like behavior, and the ERK pathway inhibition in the mPFC induced anhedonia and locomotor impairment in rats.

但值得提出的是两个脑区ERK通路在对具体的抑郁行为表现的调节上存在一定的差异，如海马ERK信号阻断引起显著的焦虑行为反应而无活力水平的降低，而前额叶皮质ERK通路阻断则表现了活力降低而无焦虑行为，从而表现了一定的脑区特异性。

The results showed that the inhibition of the ERK pathway in dHP resulted in anhedonia and anxiety-like behavior, and the ERK pathway inhibition in the mPFC induced anhedonia and locomotor impairment in rats. The phosphorylation of the cyclic AMP-responsive-element-binding protein was decreased following the ERK pathway inhibition either in dHP or mPFC.

但值得提出的是两个脑区ERK通路在对具体的抑郁行为表现的调节上存在一定的差异，如海马ERK信号阻断引起显著的焦虑行为反应而无活力水平的降低，而前额叶皮质ERK通路阻断则表现了活力降低而无焦虑行为，从而表现了一定的脑区特异性。

And more, ERK contents between group A and B, group C and D were not dramatically different. The pathological lesions indicated that intestinal tissue necrosis was severe in group C and D, which were graded 3 points, but obviously lessened in group A and B, which was graded 1 point, with ITF interfering. Conclusion: Intestinal inflammation was ameliorated after ITF was injected hypodermically or intraperitoneally.

结果：A、B组组织匀浆中ERK的面密度值各为87.68±19.24、82.65±21.35，较C、D组(30.23±7.79、30.74±8.19)明显升高(P＜0.01)，C、D组与E组(5.41±1.46)比较也有升高(P＜0.05)；并且随著ERK的激活伴随著明显的核转位。A、B组间及C、D组间ERK含量无显著差异(P＞0.05)；病理切片显示C、D组HE染色切片见肠壁损伤轻重不一，可见全肠粘膜绒毛坏死，病理评分的中位积分为3分；A、B组肠上皮细胞少量脱落，顶端绒毛坏死，病理评分的中位积分为1分。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

Furthermore, we used western blot to assay the concentration discrepancy of G0/G1 phase-associate proteins P21, P27, P53, cyclin D1, CDK4, p-Erk 1, p-Erk 2 and p-JNK. We found that P21, P27, P53 have significant elevation during 100μM Saussurea involucrate treatment, while CDK4 and p-JNK remain constant and cyclin D1, p-Erk 1, p-Erk 2 are decreased during the treatment.

此外，我们更进一步利用西方墨点法测量P21、P27、P53、cyclin D1、CDK4、 p-Erk 1、p-Erk 2及p-JNK这些与细胞周期中G0/G1期相关蛋白质表现情形，结果发现P21、P27及P53在乳癌细胞处理100μg/ml雪莲后，均有上升的趋势，CDK4及p-JNK没有变化，而cyclin D1及p-Erk 1、p-Erk 2则有下降情形。

They say their results support the hypothesis that ERK pathway activation caused by lamin abnormalities is an underlying cause of heart-muscle degeneration in EDMD and that their new results provide evidence that blocking ERK could prevent or delay the onset of heart failure in this disease.

研究者说，他们的研究结果支持了lamin蛋白质的不正常激活了ERK信道是导致Emery-Dreifuss进行性肌营养不良患者心脏肌肉退化的原因的假说。同时他们的最新研究结果，揭示抑制ERK信道能够避免或者延迟Emery-Dreifuss进行性肌营养不良实验鼠心力衰竭的发生。抑制ERK信道的药物已经在癌症患者中使用，证明是安全的。

The growth that conclusion EGCG can restrain cell of colonic cancer HT-29 apparently; its are likely the mechanism is the phosphation level that reduces EGFR and ERK, intervene EGFR-ERK signal turns thereby guide access.

结论EGCG可明显抑制结肠癌HT-29细胞的生长；其可能机制为下调EGFR和ERK的磷酸化水平，从而干预EGFR-ERK信号转导通路。

Taken together, our data showed that both the CSF-box and the octamer are important for the LPS-induced G-CSF promoter activity, moreover, the activation of MEK/ERK signaling pathway is indispensible for LPS-induced G-CSF expression in RAW264.7 macrophage.. It seems that LPS-induced activation of MEK/ERK pathway does not directly regulates NF-κB transactivity, but is essential for LPS-induced Oct-2 binding to the octmaer within G-CSF promoter and transcription activation of the G-CSF expression.

透过这些结果，我们认为MEK/ERK pathway的确参与LPS活化G-CSF表现的过程，虽然MEK/ERK pathway都影响了CSF-box以及octamer对G-CSF启动子所贡献的活性，但似乎MEK/ERK pathway的下游并非直接影响NF-κB调控基因转录的活性，而主要是影响了Oct-2对G-CSF启动子的调控。

Histamine deficiency markedly potentiated the acquisition of learning in cued and contextual fear conditioning in the HDCKO mice,but had no effect on cued and contextual fear extinction.However,histamine deficiency potentiated the inhibitory role of morphine withdrawal in cued fear extinction.Consistent with the behavioral results,morphine withdrawal decreased ERK phosphorylation in the amygdala and mPFC but not in the hippocampus of WT and HDCKO mice,and ERK might not be phosphorylad in the amygdale and mPFC of HDCKO mice after the 4th training of cued fear extinction.

但HDCKO小鼠增强了吗啡戒断对线索恐惧记忆消除的抑制作用，与行为学实验结果相一致是，，吗啡戒断能明显降低WT和HDCKO小鼠在线索恐惧记忆消除第4次训练后杏仁核和mPFC脑区的ERK磷酸化水平，但对海马脑区的ERK磷酸化没有作用；HDCKO小鼠在线索恐惧记忆消除训练的第4次训练后杏仁核、mPFC脑区的ERK蛋白没有明显磷酸化激活。

They weren't aggressive, but I yelled and threw a rock in their direction to get them off the trail and away from me, just in case.

他们没有侵略性，但我大喊，并在他们的方向扔石头让他们过的线索，远离我，以防万一。

In slot 2 in your bag put wrapping paper, quantity does not matter in this case.

在你的书包里槽2把包装纸、数量无关紧要。