查询词典 ERKS

bFGF enhances the tolerance to hypoxia of aged rat cardiomyocytes and the activation of ERKs is involved in the protective mechanism.

bFGF可以提高老年大鼠心肌细胞对于缺氧的耐受性，其保护机制涉及ERKs的活化。

The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs.

AA对BEL-7402无明显的作用，但能有效的通过caspase-3而不是ERKs的激活促进AT对肝癌细胞的凋亡效应。

Besides, the signal transduction pathway, including ERKs、JNKs and p38 involved in arsenic and its metabolites are totally different.

其中，砷化物可能透过的机转包括ERKs、 JNKs和p38三条路径，彼此间确实有明显的不同。

5-LOX participate in the formation of retinal neovascularization,Selective inhibition of 5-LOX can reduce the expression of VEGF and its receptor KDR, its specific mechanism may be associated with inhibition of ERKs signaling.

5-LOX参与视网膜新生血管的形成，通过对其选择性抑制可下调VEGF及受体KDR的表达从而抑制新生血管的生成，具体机制可能与抑制5-LOX激活MAPKs信号通路的外部ERKs有关。

Results The ERKs in myocardium treated with PTMR were activated at 2 hours and lasted to 24 hours, and the relative protein abundance of ERKs increased to a peak level from 24 hours to 7 days after operation, compared with sham-operated controls.

结果 与假手术对照组比较，PTMR实验组心肌组织内ERKs于2 h开始激活，持续至24 h；其蛋白含量于术后24 h开始升高并持续至术后7 d。

However, ischemic challenge also repressed ERKs activity when Src kinase was excessively activated.

结论致死性脑缺血刺激NMDA受体通过Src激酶和CaMKⅡ介导ERKs活性上调，但是脑缺血诱导的Src过度激活可能也参与了ERKs信号通路的负性调控。

The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs-Conclusion; Caspase-3 and ERKs proteins could involve in arsenic-induced hepatocarcinoma cell apoptosis and differentiation respectively as intracellular signaling molecules; The effect between AT and AA on hepatocarcinoma is synergistic, which further inhibits cell growth and induces apoptosis in human hepatocarcinoma cells through activation of caspase-3 but not ERRs.

AA对BEL-7402无明显的作用，但能有效的通过caspase-3而不是ERKs的激活促进AT对肝癌细胞的凋亡效应。结论：ERKs和caspse-3信号蛋白可能分别参与了砷剂诱导的人肝癌细胞促分化和凋亡效应，AT和AA对肝癌细胞的作用有协同性，他们通过caaspase-3而不是ERKs的激活进一步抑制了肝癌的生长，诱导其凋亡。

Before transfected with AT1, neither AngⅡ nor stretch increased the activation of ERKs. After transfected with AT1, pretreatment with AngⅡ for 8 min or stretch for 10 min activated ERKs obviously.

COS7细胞转染AT1受体以前， AngⅡ和牵张刺激都不能引起细胞内ERKs磷酸化升高；而转染野生型AT1后，AngⅡ和牵张刺激引起细胞内ERKs磷酸化明显升高，各突变体中，Q257A和C289A转染细胞后细胞对牵张刺激的反应受到明显抑制，提示AT1的牵张感受位点在Q257A和C289A。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and ［Ca2+］i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.（2）The activation of ERKs and the increase of ［Ca2+］i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of ［Ca2+］i, but not affect the activation of ERKs.

结果： ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及［Ca2+］i浓度，以上作用可被ETA受体拮抗剂BQ123所完全抑制，被百日咳毒素部分抑制，而ETB受体拮抗剂BQ788则无效；②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用，钙通道拮抗剂硝苯地平可明显抑制ET-1介导的［Ca2+］i浓度增加，但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应；③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活，但可抑制ET-1介导的的［Ca2+］i浓度增加及心肌细胞肥大反应。

Results By incubating cardiomyocytes with bFGF, ERKs was activated and the cellular viability 〔(70.0±4.6)%in bFGF 10 ng group vs.(53.0±4.5)%in H/R group, P＜0.01） and the ATP content 〔(23.1±2.3) nmol/106 cells in bFGF 10 ng group vs.(12.3±2.1) nmol/106 cells in H/R group, P＜0.01〕 were increased, also the LDH leakage 〔(257.3±51.0) U/L in bFGF 10 ng group vs.(372.5±69.2) U/L in H/R group, P＜0.05〕, was decreased, then attenuation of H/R injury to cardiomyocytes was observed. PD098059, an inhibitor of upstream kinase of ERKs completely abolished the protective effects 〔viability (57.0±5.8)%,ATP content (15.1±2.6) nmol/106 cells,LDH activity in medium (325.5±59.0)U/L in PD098059 group vs. bFGF 10 ng group, P＜0.01, respectively〕.

结果 bFGF激活ERKs，并呈剂量依赖性减轻H/R所致心肌细胞损伤，表现为细胞存活率〔bFGF 10 ng组(70.0±4.6)%，H/R组(53.0±4.5)%，P＜0.01〕和细胞内ATP含量〔bFGF 10 ng组(23.1±2.3)nmol/106细胞，H/R组(12.3±2.1)nmol/106细胞，P＜0.01〕升高，细胞浆酶LDH漏出〔bFGF 10 ng组（257.3±51.0）U/L，H/R组（372.5±69.2）U/L，P＜0.05〕减少；ERKs上游激酶抑制剂PD098059完全消除上述保护作用〔PD098059组细胞存活率（57.0±5.8）%，ATP含量（15.1±2.6）nmol/106细胞，培养液中LDH活性（325.5±59.0）U/L，与bFGF 10 ng组比较均为P＜0.01〕。

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。