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protein activation
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  蛋白质活性
     The calculation and characteristic analysis for the coupling solutions can explain the coupling effect of traveling wave solition solutions of the helix chain movement model for the alpha_helix protein and reveal the direction in which the protein activation and function are increased and fixed.
     耦合解组的算例函数及其特性分析,解释了α螺旋蛋白质螺旋链运动模型的行波孤立子解的耦合效应,揭示了增加、稳定和控制蛋白质活性和功能的方向。
短句来源
     The calculation cases and their characteristic analysis of coupling solutions explain the coupling effect of tra veling wave soliton solutions of the helix chain movement model of the alpha-helix protein and reve al the direction which increases and fixes and controls the protein activation and function. The resea rch methods in this paper provide ways for the traveling wave accurate solutions of the life-form brand molecule helix chain movement model.
     耦合解组的算例函数及其特性分析,解释了α螺旋蛋白质螺旋链运动模型的行波孤立子解的耦合效应,揭示了增加、稳定和控制蛋白质活性和功能的方向,文章的研究方法,为求解生物大分子螺旋链运动模型的行波精确解组探索了溪径。
短句来源
  “protein activation”译为未确定词的双语例句
     After acinar cells were pre-permeabilized with SLO for 10min, GTPγs shifted the dose-response curve of SA(I) stimulated amylase secretion to the left, decreasing EC50 from 2.0×10-5 to 1.0×10-5mol·L-1. These results suggest receptor-coupled G protein activation is involved during SA(I) stimulation of amylase secretion.
     用SLO预通透腺泡10min后 ,加入GTPγs使SA(I)刺激酶分泌的量 -效曲线左移 ,SA(I)的EC50 从2.0×10-5mol·L-1 减小到1.0×10-5mol·L-1。 以上结果提示 ,SA(I)活化受体偶联的G蛋白包括在其刺激酶分泌的信号传导通路中
短句来源
     Results 1) the HCV core protein activation of NF κB mediated STPs was inhibited by aspirin.
     结果  ( 1)HCV核心蛋白活化NF κB介导的STPs被乙酰水杨酸抑制 ;
短句来源
     CONCLUSION Inhibitory effects of HA824 and HA4 on HER-2 mRNA expressions in SK-BR-3 cells may not be associated with Caspase-3 protein activation.
     结论 HA82 4、HA4这两种靶向HER 2mRNA反义药物对SK BR 3乳腺癌细胞株增殖的抑制作用可能与激活Caspase 3蛋白无关。
短句来源
     Cloning and Expression of Vibrio cholerae CTB Gene and the Recombinant CTB Protein Activation Assay
     霍乱弧菌CTB基因的克隆、表达及重组蛋白活性分析
短句来源
     2) The IκBα dosage in the lysate of Cos 7 cells transfection with pCXN 2 core was less than that of the pCXN 2. 3) the HCV core protein activation of NF κB mediated STPs were not blocked by MEKK△.
     ( 2 )pCXN2 core转染后的细胞溶解液中IκBα的量较pCXN2 转染后的少 ;
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  相似匹配句对
     protein.
     protein。
短句来源
     It was suggested that PSS inhibits the activation of protein kinase C.
     这提示,藻酸双酯钠可抑制蛋白激酶C的激活。
短句来源
     ACTIVATION OF G PROTEIN ON THE MEMBRANE OF TCS-SENSITIVE CELLS
     天花粉蛋白引起敏感细胞膜上G蛋白激活的初步研究
短句来源
     EXERCISE AND PROTEIN
     运动与蛋白质
短句来源
     On Activation Energy
     关于“活化能”
短句来源
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  protein activation
In this research, we studied the anatomical distribution of functional receptors in young and adult animals by using the [35S]GTPγS "binding" assay as an indication of G-protein activation by CXCL12 (the natural CXCR4 ligand) or by μ-opioid agonists.
      
Subsequent to G protein activation several effectors are known to orchestrate the opioid signal.
      
Thus, our data suggest that angiotensin II-dependent tyrosine phosphorylation signaling cascades are mediated through a diverse set of signaling pathways that are partially dependent on Ca2+ mobilization and heterotrimeric G protein activation.
      
This work investigated the role of Ca2+ mobilization and heterotrimeric G protein activation in mediating angiotensin II-dependent tyrosine phosphorylation signaling patterns.
      
The role of Ca2+ mobilization and heterotrimeric G protein activation in mediating tyrosine phosphorylation signaling patterns i
      
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Objective To investigate the effect of angiotensin Ⅱ(AⅡ) on maxi conductance calcium activated potassium channel(BK Ca ) activity in ECV304 cell membrane,and the possible involvement of G protein. Methods Cell attached configuration of patch clamp technique was employed to record the current of BK Ca in ECV304. Results 10 -7 mol/L angiotensin Ⅱ inhibited the BK Ca activity. Current amplitude and open probability were decreased, open time was shortened and close time was increased. G...

Objective To investigate the effect of angiotensin Ⅱ(AⅡ) on maxi conductance calcium activated potassium channel(BK Ca ) activity in ECV304 cell membrane,and the possible involvement of G protein. Methods Cell attached configuration of patch clamp technique was employed to record the current of BK Ca in ECV304. Results 10 -7 mol/L angiotensin Ⅱ inhibited the BK Ca activity. Current amplitude and open probability were decreased, open time was shortened and close time was increased. G protein activation could eliminate the inhibition of AⅡ. Conclusions AⅡ significantly decreased the activity of BK Ca in ECV304,which might depolarize the membrane,and the stability of membrane might change. Thus endothelial cell dysfunction might be induced. G protein activation was involved in the regulation of the above AⅡ inhibition process.

目的 探讨血管紧张素 (A )对人脐静脉内皮细胞株 ECV 30 4大电导钙激活钾通道 (BKCa)的影响及 G蛋白在此过程中的作用。方法 用细胞贴附式膜片箝技术记录 BKCa的活动电流。结果  10 - 7mol/ L A 可抑制 ECV30 4细胞膜上 BKCa的活动 ,表现为电流幅值下降 ,开放概率减小 ,通道开放时间缩短 ,关闭时间延长 ;G蛋白稳定激动剂 GTPγS可对抗 A 的抑制效应 ,G蛋白稳定抑制剂 GDPβS则增强 A 的抑制效应。结论  A 可明显减弱 ECV30 4细胞膜上 BKCa的活动 ,使膜向着去极化方向发展 ,从而改变膜的稳定性 ,导致内皮细胞功能障碍。 G蛋白在此过程中起调节作用。

To elucidate the site of action of Saikosaponin (I) in pancreatic acinar cells, the modulatory effects of guanosine 5'-triphosphate(GTPγs) were investigated in SLO permeabilized pancreatic acinar cells. In a permeabilizing medium, GTPγs addition induced 15min amylase secretion, the effects being maximal at 10-7mol·L-1. GTPγs effects were concentration dependent. GTPγs 10-7mol·L-1 increased amylase secretion stimulated by 10-5mol·L-1 SA(I) 1.6 fold. After acinar cells were pre-permeabilized with SLO for 10min,...

To elucidate the site of action of Saikosaponin (I) in pancreatic acinar cells, the modulatory effects of guanosine 5'-triphosphate(GTPγs) were investigated in SLO permeabilized pancreatic acinar cells. In a permeabilizing medium, GTPγs addition induced 15min amylase secretion, the effects being maximal at 10-7mol·L-1. GTPγs effects were concentration dependent. GTPγs 10-7mol·L-1 increased amylase secretion stimulated by 10-5mol·L-1 SA(I) 1.6 fold. After acinar cells were pre-permeabilized with SLO for 10min, GTPγs shifted the dose-response curve of SA(I) stimulated amylase secretion to the left, decreasing EC50 from 2.0×10-5 to 1.0×10-5mol·L-1. These results suggest receptor-coupled G protein activation is involved during SA(I) stimulation of amylase secretion.

为了解柴胡皂甙 (I)[SA(I)]刺激大鼠胰腺腺泡酶分泌的信号传导通路 ,研究了GTPγs对SA(I)刺激通透腺泡细胞酶分泌的影响。用SLO通透细胞的同时 ,加入GTPγs在15min期间能诱发酶分泌 ,10-7mol·L-1 GTPγs有最大促泌效应。GTPγs浓度依赖性的增强SA(I)促酶分泌作用 ,10-7mol·L-1 GTPγs导致10-5mol·L-1 SA(I)刺激酶分泌量增加到1.6倍。用SLO预通透腺泡10min后 ,加入GTPγs使SA(I)刺激酶分泌的量 -效曲线左移 ,SA(I)的EC50 从2.0×10-5mol·L-1 减小到1.0×10-5mol·L-1。以上结果提示 ,SA(I)活化受体偶联的G蛋白包括在其刺激酶分泌的信号传导通路中

Objective To investigate the effect of NMDA receptor antagonist ketamine on the activation of phospho-P53 protein induced by ischemia-reperfusion in the hippocampus. Methods The model rats were subjected to four-vessel occlusion (4-VO) with some modification. The changes of phospho-P53 protein level in the hippocampus and the roles of ketamine in phospho-P53 protein activation were examined by Western blot. Results The activation of phospho-P53 protein was increased after reperfusion, reached...

Objective To investigate the effect of NMDA receptor antagonist ketamine on the activation of phospho-P53 protein induced by ischemia-reperfusion in the hippocampus. Methods The model rats were subjected to four-vessel occlusion (4-VO) with some modification. The changes of phospho-P53 protein level in the hippocampus and the roles of ketamine in phospho-P53 protein activation were examined by Western blot. Results The activation of phospho-P53 protein was increased after reperfusion, reached its peak level at 3 d, when it was 4 folds higher than that of the control rats, and then declined. Ketamine (50 mg/kg and 25 mg/kg) markedly inhibited the rising level of phospho-P53 protein. Conclusion NMDA receptor might take part in the mechanism of phospho-P53 protein activation in rat hippocampus following forebrain ischemia-reperfusion, suggesting the existance of a signal passageway of NMDA receptor→phospho-P53 protein(serine 15) activation in the process of neuronal damage after ischemia-reperfusion.

目的 研究NMDA受体拮抗剂对脑缺血再灌注诱导海马中P5 3蛋白的磷酸化激活的作用。方法 采用四动脉结扎 (4 -VO)全脑缺血模型 ,利用免疫印迹法研究缺血再灌注不同时间实验大鼠海马中P5 3磷酸化激活变化 ,以及NMDA受体拮抗剂氯胺酮对P5 3磷酸化激活的作用。结果 P5 3蛋白在缺血再灌注后丝氨酸磷酸化激活增加 ,再灌注 1天后开始上升 ,3天达到高峰 ,是假手术组的 4倍。氯胺酮剂量为 5 0mg kg和 2 5mg kg时 ,能显著抑制P5 3蛋白磷酸化激活 (P <0 .0 1)。结论 NMDA受体参与介导脑缺血再灌注诱导大鼠海马P5 3蛋白的丝氨酸磷酸化激活 ,提示NMDA受体→P5 3丝氨酸磷酸化激活信号通路可能参与脑缺血再灌注神经元损伤。

 
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