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诱导激酶
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  inducible kinase
     Conclusion SSH is an effective method to isolate differentially expressed genes. Hemorrhagic shock changes the expressions of some genes in rat heart, such as Rat 45S rDNA gene transcription initiation region, Rattus norvegicus cysteine rich protein 61 and Rattus norvegicus serum inducible kinase (Snk). But the relation between these genes and the injuries needs further study.
     结论 SSH技术是一种高效的筛选差异基因的方法 ,本实验发现失血性休克可导致大鼠 45SrDNA基因转录起始区域、鼠半胱氨酸富含蛋白 6 1及鼠血清诱导激酶等基因的差异表达 ,今后的工作中我们将进一步研究它们与失血性休克所致损伤的关系
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  “诱导激酶”译为未确定词的双语例句
     Gene expression and tenocyte proliferation of nuclear factor-κB under the stimulation of basic fibroblast growth factor
     核因子-κB诱导激酶和IκB激酶在碱性成纤维细胞生长因子作用下基因表达及肌腱细胞增殖
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     Study of CD4~+CD25~+ regulatory T cells in NIK mutated mice
     NF-κB诱导激酶基因突变对CD4~+CD25~+调节性T细胞产生的影响
短句来源
     Upon recognizing respective ligand, TLR recruits adapter protein, myeloid differentiation protein 88 (MyD88), and activates mitogen-activated protein kinases (MAPKs) and nuclear factor-KB (NF-kB) through MyD88/IRAK /TRAF6/TAK1 kinases cascade.
     TLR9识别配体后,通过MyD88-IRAK-TRAF6激酶途径募集接头蛋白髓系分化蛋白88(MyD88),结合并活化IL-1受体相关激酶(IRAKs)、肿瘤坏死因子受体相关因子6(TRAF6),活化下游MAPKs和NF-κB诱导激酶(NIK)、IKK、IκBa,活化后的NF-κB入核引起特定基因的表达。
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     Serum-inducible kinase (SNK), one of the polo-like kinases, induced by synaptic activity and was targeted to dendritic spines, eliminates SPAR protein, and causes loss of mature dendritic spines and synapses.
     在神经元活化时SPAR可被血清诱导激酶(serum-inducible kinase, SNK)降解,从而导致树突棘结构的失稳定。
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     Both NF κB inducing kinase(NIK) and mitogen activated protein kinase kinase kinase 1(MEKK 1) are upstream kinases of IKK. MEKK 1 preferentially activates IKK β,whereas NIK efficiently phosphorylates both IKK α Ser176 and IKK β.
     核因子κB诱导激酶 (NIK)与丝裂原活化蛋白激酶激酶激酶 1(MEKK1)均为IKK的上游激酶 ,NIK可引起IKK αSer176、IKK β相应位点的磷酸化 ,而MEKK1主要引起IKK β的活化 .
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     The role of protein kinase C in the formation of cerebral ischemic tolerance induced by isoflurane preconditioning
     蛋白激酶C在异氟醚诱导脑缺血耐受中的作用
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     Study on the apoptosis in CNE-2Z cells induced by inhibitors of protein kinase C
     蛋白激酶C抑制剂诱导CNE-2Z细胞凋亡的研究
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     in troducing stimulus;
     诱导刺激;
短句来源
     POLYPLOID INDUCEMENT OF Eucommia ulmoides
     杜仲多倍体的诱导
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     adjustment of protein kinase C;
     调节蛋白激酶C;
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  inducible kinase
Significance and expression of Serum and Glucocorticoid-inducible Kinase in kidney of mice with diabetic nephropathy
      
To investigate the expression and the role of three isoforms of Serum and Glucocorticoid-inducible Kinase (SGK) in experimental diabetic nephropathy (DN), 12 male C57BL/6 mice of 8-weeks-old were divided into two groups.
      
Expression of serum and glucocorticoid-inducible kinase1 in diabetic rats and its modulation by fluvastatin
      
Mineralocorticoids have been shown to upregulate the serum- and glucocorticoid-inducible kinase 1 (SGK1), which participates in the effects of mineralocorticoids on renal tubular Na+ reabsorption and salt appetite.
      
The effects of mineralocorticoids on renal tubular Na+ reabsorption and salt appetite involve the serum- and glucocorticoid-inducible kinase 1 (SGK1).
      
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During the course of NF κB dimer activation, IκB kinase(IKK) play a crucial role by phosphorylation of inhibitory κB(IκBs). There are lots of existing forms in cytoplasm about IKK complex, which activate IκBs through different ways. Generally, IKK has two catalytic subunits, IKK α?IKK β, which have 52% amino acids identity and similar construction, one regulatory subunit, IKK γ. Both NF κB inducing kinase(NIK) and mitogen activated protein kinase kinase kinase 1(MEKK 1) are upstream kinases of IKK....

During the course of NF κB dimer activation, IκB kinase(IKK) play a crucial role by phosphorylation of inhibitory κB(IκBs). There are lots of existing forms in cytoplasm about IKK complex, which activate IκBs through different ways. Generally, IKK has two catalytic subunits, IKK α?IKK β, which have 52% amino acids identity and similar construction, one regulatory subunit, IKK γ. Both NF κB inducing kinase(NIK) and mitogen activated protein kinase kinase kinase 1(MEKK 1) are upstream kinases of IKK. MEKK 1 preferentially activates IKK β,whereas NIK efficiently phosphorylates both IKK α Ser176 and IKK β. Through cascade reaction, IκBs are phosphorylated by IKK and dissociated from IκB NF κB complex, NF κB dimer enter the nucleus and activate a series of genes.

在NF κB二聚体活化过程中 ,IκB激酶 (IKK)通过对抑制性蛋白κB (IκBs)的磷酸化而扮演关键的角色 .IKK复合物在胞浆内有多种存在形式 ,其中 ,IKK α、IKK β两者氨基酸序列 5 2 %的同源性 ,空间构象相似 ,常为催化亚单位 ,而IKK γ则为调节亚单位 ,它们以不同的方式活化IκBs.核因子κB诱导激酶 (NIK)与丝裂原活化蛋白激酶激酶激酶 1(MEKK1)均为IKK的上游激酶 ,NIK可引起IKK αSer176、IKK β相应位点的磷酸化 ,而MEKK1主要引起IKK β的活化 .通过级联反应 ,使IκBs磷酸化而与NF κB解离 ,致使NF κB被激活并易位入核 ,启动免疫及炎症相关的基因转录

Objective To investigate the signal transduction pathway of NF-kB activated by minimally modified low density lipoprotein(mm-LDL)in endothelial cells and the effect of NF-kB on platelet derived growth factor b(PDGFb)mRNA expression. Methods mm-LDL was prepared through iron oxidation by dialyzing the native LDL against FeSO4 in PBS. Endothelial cells were incubated in a medium containing mm-LDL, TNF, and IL-1 respectively and electrophoretic mobility shift assay (E- MSA)was displayed to check on the activation...

Objective To investigate the signal transduction pathway of NF-kB activated by minimally modified low density lipoprotein(mm-LDL)in endothelial cells and the effect of NF-kB on platelet derived growth factor b(PDGFb)mRNA expression. Methods mm-LDL was prepared through iron oxidation by dialyzing the native LDL against FeSO4 in PBS. Endothelial cells were incubated in a medium containing mm-LDL, TNF, and IL-1 respectively and electrophoretic mobility shift assay (E- MSA)was displayed to check on the activation of NF-kB. Luciferase reporter gene was analysed to investigate the effect of nuclear factor inducing kinase(NIK)、inhibitor of NF-kB kinase α(IKKα)and inhibitor of NF-kB kinase β(IKKβ) on NF-kB activation. In addition,endothelial cells were transfected using PDGFb promoter-luciferase for reporter gene analysis or transfected with mut-NIK for slot blot analysis to study the effect of NF-kB on PDGFb mRNA expression. Results mm-LDL was able to activate NF-kB in endothelial cells. mut-NIK and mut-IKKβ inhibited lucifer-ase activity induced by mm-LDL. mm-LDL could also enhance luciferase activity controled by upstr-eam sequence of PDGFb promoter which contains element interacting with NF-kB. Result of slot blot showed inhibition of PDGFb mRNA expression by mut-NIK in the endothelial cells stimulated by mm-LDL. Conclusion mm-LDL may activate NF-kB through NIK-IKKβ pathway and promote PDGFb mRNA expression in endothelial cells.

目的 研究轻微修饰低密度脂蛋白(mm-LDL)激活内皮细胞转录因子NF-kB的信号传导途径以及NF-kB对血小板源性生长因子B链(PDGFb)表达的调控作用。方法 以FeSO4修饰法制备mm-LDL,以正常LDL(n-LDL)作对照,作用于培养内皮细胞后提取核蛋白,用凝胶阻滞实验检测转录因子NF-kB核转位及结合活性的变化。观察自由基清除剂probucol及PDTC对mm-LDL激活内皮细胞转录因子NF-kB的影响。通过检测报告基因探讨核因子诱导激酶(NIK)和核因子-kB抑制亚基激酶(IKK)在激活内皮细胞转录因子NF-kB的信号传导途径中的作用以及mm-LDL激活的NF-kB对PDGFb基因启动子的作用。结果 mm-LDL能激活培养内皮细胞转录因子NF-kB, 自由基清除剂probucol和PDTC对mm-LDL激活内皮细胞转录因子NF-kB无明显抑制作用。变异型NIK及IKK能显著降低报告基因荧光素酶的活性,mm-LDL激活的NF-kB还能增加带有PDGFb基因上游调控序列(-189/+43)的报告基因荧光素酶的活性。Slot blot结果显示变异型NIK能显著减少受mm-LDL刺激的内皮细...

目的 研究轻微修饰低密度脂蛋白(mm-LDL)激活内皮细胞转录因子NF-kB的信号传导途径以及NF-kB对血小板源性生长因子B链(PDGFb)表达的调控作用。方法 以FeSO4修饰法制备mm-LDL,以正常LDL(n-LDL)作对照,作用于培养内皮细胞后提取核蛋白,用凝胶阻滞实验检测转录因子NF-kB核转位及结合活性的变化。观察自由基清除剂probucol及PDTC对mm-LDL激活内皮细胞转录因子NF-kB的影响。通过检测报告基因探讨核因子诱导激酶(NIK)和核因子-kB抑制亚基激酶(IKK)在激活内皮细胞转录因子NF-kB的信号传导途径中的作用以及mm-LDL激活的NF-kB对PDGFb基因启动子的作用。结果 mm-LDL能激活培养内皮细胞转录因子NF-kB, 自由基清除剂probucol和PDTC对mm-LDL激活内皮细胞转录因子NF-kB无明显抑制作用。变异型NIK及IKK能显著降低报告基因荧光素酶的活性,mm-LDL激活的NF-kB还能增加带有PDGFb基因上游调控序列(-189/+43)的报告基因荧光素酶的活性。Slot blot结果显示变异型NIK能显著减少受mm-LDL刺激的内皮细胞 PDGFb mRNA含量。结论 mm-LDL可通过NIK-IKK途径激活内皮细胞转录因子NF-kB并促进PDGFb基因表达。

Objective To investigate genetic clues to reveal the mechanisms of severe heart injuries caused by hemorrhagic shock, especially by hypoxia and ischemia in rats. Methods Hemorrhagic shock rat models were established and total RNA were extracted from rat hearts. After the synthesis of the dscDNA, differentially expressed genes was isolated with suppression subtractive hybridization (SSH). Then the isolated genes were cloned and sequenced. The sequencing results were compared with their counterparts in Genbank...

Objective To investigate genetic clues to reveal the mechanisms of severe heart injuries caused by hemorrhagic shock, especially by hypoxia and ischemia in rats. Methods Hemorrhagic shock rat models were established and total RNA were extracted from rat hearts. After the synthesis of the dscDNA, differentially expressed genes was isolated with suppression subtractive hybridization (SSH). Then the isolated genes were cloned and sequenced. The sequencing results were compared with their counterparts in Genbank to search for their homology. Results Among the 42 obtained positive genes, 25 were highly expressed and 17 lowly. Additionally, 5 new sequences were found. Conclusion SSH is an effective method to isolate differentially expressed genes. Hemorrhagic shock changes the expressions of some genes in rat heart, such as Rat 45S rDNA gene transcription initiation region, Rattus norvegicus cysteine rich protein 61 and Rattus norvegicus serum inducible kinase (Snk). But the relation between these genes and the injuries needs further study.

目的 失血性休克可导致大鼠心肌的缺血、缺氧 ,进而对心肌细胞造成严重损伤 ,本实验将利用抑制性消减杂交技术(Suppressionsubtractivehybridization ,SSH) ,研究失血性休克大鼠心肌的差异表达基因 ,以期通过基因线索寻找其损伤机制。方法 建立失血性休克大鼠模型 ,选其心肌 ,提取总RNA ,构建cDNA文库 ,应用抑制性消减杂交技术筛选其差异表达基因。通过反向North ern杂交验证差异表达基因阳性克隆 ,并进行测序分析 ,登陆Genbank寻找同源性基因。结果 获得 42个阳性结果 ,2 5个为高表达基因 ,17个为低表达基因 ,其中发现 5个新的cDNA片段。结论 SSH技术是一种高效的筛选差异基因的方法 ,本实验发现失血性休克可导致大鼠 45SrDNA基因转录起始区域、鼠半胱氨酸富含蛋白 6 1及鼠血清诱导激酶等基因的差异表达 ,今后的工作中我们将进一步研究它们与失血性休克所致损伤的关系

 
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