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gi protein
    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。
    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
    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。
    Furthermore,TLR2,Gi protein,PKC and several selective splicing isoforms are involved in endotoxin tolerance.
    除此之外,TLR2通路、G i蛋白、蛋白激酶C(protein kinase C,PKC)以及一些信号分子的剪接异构体等也参与了内毒素耐受现象的发生。
    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.
    It is concluded that the depressant effect of IL 2 on the contractility of isolated ventricular myocytes is mainly mediated by cardiac κ opioid receptor pathway including a PTX sensitive Gi protein and PLC.
    结果表明 ,IL 2对酶解分离心室肌细胞收缩的抑制作用 ,是通过心肌细胞上κ阿片受体介导的 ,其下游途径包括PTX敏感的Gi蛋白和磷脂酶C
    RT PCR revealed no significant change in mRNA of κ opioid receptor. Western blot showed no change in Gi protein. While biologically active Gs small protein decreased significantly.
    κ 阿片受体mRNA的表达和Gi蛋白的活性在慢性缺氧后无明显改变 ,而小Gs蛋白的活性明显降低。
    BRL37344 decreased beating rate and intracellular cAMP levels. PTX, Gi protein inhibitor and Bupranolol, nonspecific β-ARs antagonist totally blocked the effect and L-NAME, nitric oxide synthase (NOS) inhibitor partly blocked the effect, but Nadolol did not.
    BRL 37344可显著降低心肌细胞搏动频率和cAMP含量 ,这种作用可被PTX(Gi 蛋白抑制剂 )和Bupranolol(非选择性 β受体阻滞剂 )完全阻断 ,同时可被L NAME(一氧化氮合酶抑制剂 )部分阻断 ,不受Nadolol影响。
    Furthermore, it was n oticeable that the I-V shift of sodium channel in PTX-treated neurons was significantly similar to that of resistant cotton bollworm, which indicated that Gi protein might participate in the evolution of resist ance to insecticide.
    同时,经百日咳毒素处理后钠通道的I-V曲线与抗性棉铃虫I-V曲线非常相似,可能暗示Gi蛋白在棉铃虫抗药性形成中发挥作用。
    The gene transcription of the α subunit of Gi protein in the hippocampus of the rats with hypertensive cerebral hemorrage on different phases after electroaupuncture treatment were detected with northern blotting.
    运用Northernblotting分子杂交技术动态检测电针治疗后不同时相点脑出血大鼠海马Gi蛋白α亚基基因转录水平。
 

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