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    THE HYPERFUNCTION OF THYROID AUTONOMOUS NODULE IS HIGHLY ASSOCIATED WITH SENSITIVITY OF TSH RECEPTOR AND FUNCTIONAL CHARACTERISTICS OF Gs/Gi
    自主性甲状腺结节的高功能与TSH受体的敏感性及Gs/Gi蛋白功能特性的关系
    Involvement of Giβγ subunits in carbacholstimulated phospholipase A2 activation in CCL137 cells
    Gi蛋白βγ亚单位在氨甲酰胆碱所致CCL137细胞磷脂酰A_2激活中的作用
    EFFECT OF β_1 INTEGRIN AND ITS BINDING CYTOSKELETON ON Gi DISTRIBUTION IN CARDIOMYOCYTES
    β1整合素及细胞骨架结构对Gi蛋白心肌细胞内构型的影响
    RT-PCR, Western blotting, Northern blotting and immunohistochemical method on the content or express of T3NRmRNA, Gsα, Gi α, Go α, Goα mRNA and SS;
    运用RT-PCR、Western blotting、Northern blotting,免疫组化等技术分别检测其海马T_3MRmRNA、Gs蛋白α亚基、Gi蛋白α亚基、Go蛋白α亚基的含量,GoαmRNA及SS的表达;
    The pathological changes of Gi a, Go a, Gi a mRNA, cAMP, SS and SSmRNA in hippocampus of hypertensive cerebral hemorrhage model rats indicate that there is the disorder of signal transduction in neuroendocrine system.
    实验性高血压性脑出血大鼠海马出现Gi蛋白α亚基、Go蛋白α亚基、GiαmRNA、cAMP、SS、SSmRNA等的病理变化,表明脑出血时存在着生物信号转导机制等方面的神经内分泌代谢功能紊乱。
    Newly discovered regulator of G-protein signaling (RGS) is a GTPase activating protein (GAP). It can accelerate GTP hydrolyzing of Giα and Gqα, consequently reduce the intensity and duration of Gq and Gi protein activation, and adjust the signal pathway.
    近年发现的G蛋白信号转导调节因子(Regulators of G-protein signaling)是细胞内GTP酶(GTPase)激活蛋白(GTPase activating proteins,GAPs),它可加速Giα和Gqα水解GTP,从而限制Gq和Gi蛋白激活的强度和持续时间,调节信号转导过程。
    Our findings indicate that the endogenous histamine might be involved in the modulation of cardiac sympathetic neurotransmission by interacting with histamine H3-receptors and the receptors are probably coupled to a G0/Gi protein.
    以上结果表明,组胺H_3受体参与调节心交感神经冲动的传递,H_3受体可能与G0/Gi蛋白相耦联,内源性组胺经H_3受体介导参与调节心交感神经冲动的传递。
    CONCLUSIONS MT can increase the proliferation of RA patients PBL. PT Senstitive Gi protein cAMP signal transduction may be one of important mechnisms of MT in regulationg immune responses.
    结论MT可促进RA病人PBL的增殖反应,PT敏感的Gi蛋白cAMP信号转导机制参与了MT上调PBL的作用
    the PKA activator forskolin and Gi protein inhibitor pertussis toxin did not show influence on the 14.2 kD protein phosphorylation.
    PKA 激活剂佛斯可林(forskolin) 和Gi 蛋白抑制剂百日咳毒素对上述磷酸化无明显影响。
    The changes mentioned above are effectively abolished when p bromoacetophenone (PBA), pertussis toxin (PTX), dexamethasone (DEX) ,anti Giα and anti Gβγ serum are involved respectively in the reaction system .
    上述现象可分别被PLA2 特异性抑制剂对溴乙酰酚 (PBA)、地塞米松 (Dex)、Gi蛋白灭活剂百日咳毒素 (PTX)、抗Giα血清和抗Gβγ血清所抑制 ;
    CONCLUSION β 1 integrin deletion altered intracellular distribution of G i protein and it implied that signal transduction mediated by G i protein could be also influenced by β 1 integrin deficiency.
    结论 β1整合素能够影响信号分子Gi蛋白的细胞内定位 ,推测β1整合素可通过改变Gi 的分布而影响Gi 介导的信号传导
    Conclusion PT-sensitive Gi protein deals with the PBL abonrmal proliferation in SLE patients. [
    结论 PT敏感的Gi蛋白 -cAMP信号机制参与了SLE患者PBL的异常增殖反应
    As a result, acute β1AR stimulation activates the Gs-adenylyl cyclase-cAMP-PKA signaling that can broadcast throughout the cell, whereas β2AR-evoked cAMP signaling is spatially and functionally compartmentalized, due to concurrent Gi activation.
    短时间激动β1AR,使Gs蛋白-腺苷酸环化酶-环苷腺酸-蛋白激酶A(Gs-adenylyl cyclase-cAMP-PKA)信号体系激活并广布于细胞内,而激动β2AR则同时激活Gi蛋白而产生空间及功能局限的cAMP信号;
    The cardiac protective effect of β2AR is mediated by a signaling pathway sequentially involving Gi, Gβγ, PI3K and Akt.
    β2AR的心肌保护作用是通过激活Gi蛋白-Gβr-PI3K-Akt途径介导。
    In the secretory function of complement stimulated M, Gi protein has a major role in the production of NO, Gs protein is mainly involved in the secretion of TNF-α.
    其中对PM生成NO的调控主要是通过Gi蛋白途径发挥作用,对PM分泌TNF-α的调控则以Gs蛋白信号通路为主。
    The myoinhabitory role of allatostatins may be mediated by a Gi-protein, which may be different from the receptor coupling with AS to inhibit the activity of CA.
    AS对肌肉收缩的抑制的作用可能由一个Gi蛋白受体介导,且这类受体与AS抑制CA活性时的受体可能完全不同。
    Activation of PLA2 is regulated by many signaling pathways: Gi-protein, diacylglycerol, protein kinase A, proterin kinase C, mitogen-activated protein kinase and reaction oxygen species. In addition, the crosstalk between PLA2 and phospholipase C may occur by mediating of endogenous diacylglycerol.
    天然激动剂引起PLA2激活受Gi蛋白、甘油二酯、蛋白激酶A、蛋白激酶C、促分裂原蛋白激酶和活性氧等多条信号通路的调节,此外,磷脂酶A2与特异性磷酯酶C之间可以发生信号串话。
    The results showed that the above migration process was markedly diminished by PTX (inhibitor of Gi protein),U73122 (inhibitor of PLC), Staurosporine (inhibitor of PKC ), PD98059 (inhibitor of ERK1/2) and SB203580(inhibitor of p38), and lightly by SP600125 (inhibitor of JNK).
    结果显示,PTX(Gi蛋白抑制剂)、U73122(PLC抑制剂)、staurosporine(PKC抑制剂)、PD98059(ERK1/2抑制剂)和SB203580(p38抑制剂)分别可拮抗上述AA诱导的SM3细胞迁移作用,而SP600125(JNK抑制剂)的作用较弱.
    Taken together, it suggests that the signaling pathways are related to promoting the membrane translocation of PLCβ_2 by AA-activated Gi protein, furthermore resulting in migration of SM3 cells through enhancing phosphorylation levels of PKC (ε), ERK1/2, p38 and JNK, when phosphorylation of MLC20 was inhibited.
    上述结果表明,当肌球蛋白轻链的磷酸化被抑制后,AA可通过Gi蛋白的活化促进PLCβ2向细胞膜移位,进而通过激活PKC(ε)、ERK1/2、p38和JNK等信号转导途径而诱导SM3细胞发生迁移.
    ALTERATIONS OF CARDIAC G_i PROTEIN ALPHA SUBUNITS DURING ISCHEMIA-REPERFUSION IN RATS
    缺血-再灌注时大鼠心脏Gi蛋白α亚基的变化
 

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