查询词典 JUN

Experiments show that Ang Ⅱ activates JNK mediated by AT〓, and JNK increases transcription activity of c-Jun by phosphorylating c-Jun amido-terminal, and induces expression of c-Fos gene. c-Jun and c-Fos form transcriptional factor activated protein-1 complex. AP-1 may stimulates genes which correlate with cardiovascular remodeling expression, such as transforming growth factor, collagen type Ⅰ and Ⅲ, skeletal muscle α-actin,β-MHC, atrial natriuretic factor.

实验表明，在心肌和血管平滑肌细胞Ang Ⅱ通过AT〓介导激活JNK；JNK通过磷酸化c-Jun氨基末端增加c-Jun的转录活性并诱导c-Fos基因表达，c-Jun和c-Fos蛋白形成转录因子复合物激活蛋白-1(AP-1)，并刺激各种心血管重塑相关基因如转化生长因子-β1(TGF-β1)、Ⅰ，Ⅲ型胶原、骨骼肌α-actin、β-MHC(β-myosin heavy chain，β-肌球蛋白重链)、心钠素的表达。

This finding corresponded to the immunohistochemical data showing the presence of phosphorylated forms of p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase during ameloblast differentiation.

这个发现与免疫组织化学数据相符，显示在成釉细胞的分化过程中，p38磷酸化形式，c-Jun氨基端激酶以及细胞外信号调节激酶均有表达。

Our study shows a contrastive results with Jun (1996), where atonal languages such as Korean, French, and English.

我们的结果与 Jun (1996)针对韩语、法语、与英语等非音调语言所做的研究相反。

Results The expression of FOS,JUN,bFGF,and VEGF protein of the cere...

结果正常小鼠脑组织FOS、JUN、bFGF、VEGF低水平表达，B组略强。A组脑组织FOS和JUN的表达具有时程的一致性，创伤性脑损伤后3 h达到高峰，12 h以后降至对照水平；bFGF与VEGF分别于创伤性脑损伤后12 h、24 h达到高峰，72 h降至对照水平。

Winter by means of radioimmunology and in situ hybridazation to probe into the modulation mechanisms of kidney responsing to the winter, and observed effects of pinealectomy. The results show that there are seasonal changes in the level of MT in the Pineal body, serum, hyperthalamus-pituitary-gonadal axis and the same of the third courier---c-fos and the c-jun mRNA expressions in the hyperthalamus-pituitary-gonadal axis from the Summer to the Winter.

首次通过实验，观察了雄性SD大鼠在生理状态下松果体、血清、下丘脑-垂体-睾丸轴褪黑素含量的冬夏变化，下丘脑-垂体-睾丸轴第三信使（c-fos和c-jun）mRNA表达的冬夏变化以及摘除松果体对上述各项指标冬夏变化的影响，实验结果表明，松果体、血清、下丘脑-垂体-睾丸轴褪黑素含量以及下丘脑-垂体-睾丸轴第三信使（c-fos和c-jun）mRNA表达都存在明显的季节性变化。

Results A dense accumulation of fos and jun-positive neurons exhibited in the PVN, SON and DG, and some of fos and jun-positive neurons were also present in other hypothalamus and hippocampus areas including parvocellular PVN, dorsomedial nucleus and lateral hypothalamic area.

结果 游泳应激结束后3h，室旁核和视上核及齿状区内可见密集深染的c-fos和c-jun阳性细胞，室旁核小细胞部，背内侧核等区域亦有疏密不一的阳性胞体。

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。

Methods The nitroglycerin experimental migrainous animal model was reconstructed for the expression of c-fos and c-jun by means of immunohistochemical method Results The nitroglycerin experimental migrainous rats appeared reddish two ears, head shaking,scratching head with forepaws, activity increasing, both the number increasing and the area enlarging of the positive cells of the expression of c-...

免疫组化ABC法研究偏头痛大鼠脑组织即刻早期基因c -fos、c -jun的表达。结果硝酸甘油型实验性偏头痛大鼠出现双耳发红、甩头、前肢频繁搔头，活动增加等外在表现，脑组织c -fos、c -jun基因表达阳性细胞数增加，基因表达阳性细胞的面积扩大、灰度降低或变化不大。结论硝酸甘油型实验偏头痛大鼠模型复制方法简单、重复性较好、脑组织c -fos和c -jun基因异常表达明显，可以作为偏头痛治疗药物筛选、药效评价和发病机理研究的动物模型。

PPARα ligands suppressed OPN promoter actiity, and an actiator protein-1 consensus site conferred this repression. Oerexpression of c-Fos and c-Jun reersed the inhibitory effect of PPARα ligands on OPN transcription, and, in chromatin immunoprecipitation assays, PPARα ligands inhibited c-Fos and phospho–c-Jun binding to the OPN promoter.

PPARα配体可抑制OPN启动子活性，一个激活蛋白-1的一致序列位点与这种抑制有关。c-Fos和c-Jun的过表达可逆转 PPARα配体对OPN转录的抑制作用，并且在免疫沉淀实验中，PPARα配体可抑制c-Fos及磷酸化c-Jun与OPN启动子的结合。

Objective To study the statement of immunoreaction of c Jun and functional recovery of spinal cord injury in rats after fetal spinal cord transplantation.Methods Experimental rats were divided into two groups:spinal cord hemisection injury combination with transplants of FSC to injured site group,and spinal cord injury that received gelfoam pledgets group.On the lst,3th,7th,14th and 28th day after operation,6 animals in each group at each time phase,were observed for their function recovery with the methods of praxiology and electro physiological examination,the animals were then sacrificed for the observation of the statement of c Jun reaction by immnochemistry method and computer image analysis system was used for quantitative analysis.

目的：研究大鼠胚胎脊髓移植后能否影响，c-Hun免疫反应的表达和脊髓损伤后大鼠功能的恢复，方法；将动物分为脊髓半切洞损伤加胚胎脊髓移植组和单纯脊髓板切洞损伤加明胶海绵填塞组，每个时相点每组6只动物，术只1，3，7，14和28天，应用行为学和电生理检查观察大鼠功能恢复情况，应用免疫细胞化学方法，c-Jun免疫反应的表达，采用计算机图像分析技术，进行定量分析。

The physiology of the skin machine body for the sake of the environment in the maintenance stability, but eject a body metabolism creation of metabolism thing BE'grease', summer perspire many various skin disease light or good, autumn perspire little metabolism thing metabolism don't go out, various skin disease made, this be the skin machine body of various burning disease.

皮肤机体的生理为了维持内环境稳定，而排出身体代谢产生的代谢物是'油泥'，夏天出汗多各种皮肤病就轻或好了，秋天出汗少代谢物代谢不出去，各种皮肤病就犯了，这就是皮肤机体的各种炎症。

If I had anything tender in me, I shot it dead.

如果我有什么招标的话，我枪死亡。