Abstract:SummaryProteins from unrelated pathogens, including some RNA or DNA viruses and bacteria can recruit and activate cellular p90-ribosomal protein S6 kinases (RSKs) through a common linear motif. Data suggested a model where pathogens’ proteins act to dock the recruited RSKs toward specific substrates, which then act as effectors to the benefit of the pathogens. Using cardiovirus leader protein (L) as a paradigm, we show that pathogens’ proteins can modify the spectrum of RSK substrates in infected cells. L trig… Show more
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