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首页> 外文期刊>Journal of receptor and signal transduction research >Reversible translocation of ASK1 to a Triton-X100 insoluble cytoplasmic compartment during cardiac myocyte cell stress
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Reversible translocation of ASK1 to a Triton-X100 insoluble cytoplasmic compartment during cardiac myocyte cell stress

机译:心肌细胞应激期间ASK1可逆转位至Triton-X100不溶性细胞质区室

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摘要

ASK1 is a cellular stress-responsive MAPKKK which activates the JNK and p38 MAPK pathways that play a key role in the response of cardiac myocytes to redox stress following ischemia/reperfusion. ASK1 becomes incorporated into high-molecular weight complexes upon activation but this has not been investigated in cardiac myocytes. Here we examine the distribution of ASK1 in neonatal rat cardiomyocytes undergoing simulated ischemia and reperfusion. Simulated ischemia or redox stress in neonatal cardiac myocytes causes the translocation of ASK1 to distinct punctate cytoplasmic structures that are insoluble in Triton X-100. The translocation event is not dependent on ASK1 kinase activity, occurs subsequent to activation and is reversible upon removal of the cell stress. The structures to which ASK1 translocates in cardiac myocytes do not appear to correspond to the previously described ASK1 signalosome reported in other cell types.
机译:ASK1是一种细胞应激反应性MAPKKK,可激活JNK和p38 MAPK途径,这些途径在缺血/再灌注后心肌细胞对氧化还原应激的反应中起关键作用。 ASK1在激活后就被掺入了高分子量复合物中,但尚未在心肌细胞中进行研究。在这里,我们检查了ASK1在经历模拟缺血和再灌注的新生大鼠心肌细胞中的分布。新生儿心肌细胞中的模拟缺血或氧化还原应激会导致ASK1易位至不溶于Triton X-100的独特的点状细胞质结构。易位事件不依赖于ASK1激酶活性,在激活后发生,并且在去除细胞应激后可以逆转。 ASK1在心肌细胞中易位的结构似乎与其他细胞类型中报道的先前描述的ASK1信号小体相对应。

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