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Convergence of the SUMO and MAPK pathways on the ETS-domain transcription factor Elk-1

机译：ETS域转录因子ELK-1上的SUMO和MAPK路径的融合

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The ETS-domain transcription factor Elk-1 is regulated by phosphorylation in response to activation of the MAPK (mitogen-activated protein kinase) pathways.This phosphorylation triggers a series of molecular events that convert Elk-1 from a transcriptionally silent state into a highly active state and then back to a basal level.At the same time,activation of the ERK (extracellular-signal-regulated kinase) MAPK pathway leads to loss of modification of Elk-1 by SUMO (small ubiquitin-related modifier).As SUMO imparts repressive properties on Elk-1,ERK-mediated SUMO loss leads to de-repression at the same time as the ERK pathway promotes activation of Elk-1.Thus a two-step mechanism is employed to convert Elk-1 into its fully activated state.Here,the molecular events underlying these changes in Elk-1 status,and the role of PIASxa [protein inhibitor of activated STAT (signal transducer and activator of transcription) x alpha] as a co-activator that facilitates this process,are discussed.
机译：ETS-结构域转录因子ELK-1通过磷酸化响应于MAPK（丝裂原激活的蛋白激酶）途径而受到磷酸化。本磷酸化触发一系列分子事件，将ELK-1从转录静音状态转换成高度活跃状态，然后回到基础水平。同时，ERK（细胞外信号调节激酶）MAPK途径的激活导致SUMO（小泛素相关修饰符）.AS SUMO的eLK-1的变性丧失在ELK-1上赋予压抑性能，ERK介导的SUMO损失导致脱垢，同时随着ERK途径促进ELK-1.THUS的激活，使用两步机构将ELK-1转换为完全活化讨论了eLK-1状态下这些变化的分子事件，以及PiAsxa [蛋白质抑制剂（转录的转录器和活化剂和活化剂的激活剂）Xα]作为促进该过程的共激活剂的作用，是有利于该过程的。

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