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首页> 外文期刊>The Journal of Experimental Biology >Regulation of the mitogen-activated protein kinase p44 ERK activityduring anoxia/recovery in rainbow trout hypodermal fibroblasts
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Regulation of the mitogen-activated protein kinase p44 ERK activityduring anoxia/recovery in rainbow trout hypodermal fibroblasts

机译:虹鳟皮下成纤维细胞缺氧/恢复过程中丝裂原活化蛋白激酶p44 ERK活性的调节

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It is well known from various mammalian cells that anoxia has a major impact on the mitogen-activated protein kinase ERK, but a possible similar effect in fish cells has not been investigated. Here we characterise a p44ERK-like protein in the rainbow trout cell line RTHDF and study the effect of (i) serum stimulation, (ii) sodium azide (chemical anoxia) and removal of azide (recovery) and (iii) anoxia (P sub(O)20.1%) and recovery. During both chemical and true anoxia p44ERK was inhibited and recovery resulted in robust reactivation of p44ERK activity, far above the initial level. The inhibition was secondary to activation of p38 super(MAPK) and the increase was MEK dependent, as SB203580 inhibited the dephosphorylation during anoxia and the presence of PD98059 inhibited phosphorylation of p44ERK during recovery. In addition, we demonstrated that the reactivation of p44ERK during recovery also was dependent on reactive oxygen species and a PP1/PP2A-like phosphatase.
机译:从各种哺乳动物细胞中众所周知,缺氧对有丝分裂原活化的蛋白激酶ERK有重要影响,但是尚未研究在鱼类细胞中可能的类似作用。在这里,我们表征虹鳟鱼细胞RTHDF中的p44ERK样蛋白,并研究(i)血清刺激,(ii)叠氮化钠(化学性缺氧)和去除叠氮化物(回收率)和(iii)缺氧(P亚型)的作用(O)2 <0.1%)和回收率。在化学性缺氧和真正的缺氧过程中,p44ERK均被抑制,并且恢复导致p44ERK活性的强烈活化,远高于初始水平。抑制作用是继p38 super(MAPK)激活之后的,其增加是MEK依赖性的,因为SB203580抑制了缺氧过程中的去磷酸化,而PD98059的存在则抑制了恢复过程中p44ERK的磷酸化。此外,我们证明了在恢复过程中p44ERK的重新活化也取决于活性氧和PP1 / PP2A样磷酸酶。

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