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ERK and RSK regulate distinct steps of a cellular program that induces transition from multicellular epithelium to single cell phenotype
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SYSNO ASEP 0422123 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title ERK and RSK regulate distinct steps of a cellular program that induces transition from multicellular epithelium to single cell phenotype Author(s) Čáslavský, Josef (MBU-M)
Klímová, Zuzana (MBU-M) RID, ORCID
Vomastek, Tomáš (MBU-M) RID, ORCIDSource Title Cellular Signalling. - : Elsevier - ISSN 0898-6568
Roč. 25, č. 12 (2013), s. 2743-2751Number of pages 9 s. Language eng - English Country US - United States Keywords MAPK/ERK ; RSK ; Polarity Subject RIV EE - Microbiology, Virology R&D Projects GA204/09/0614 GA ČR - Czech Science Foundation (CSF) GA13-06405S GA ČR - Czech Science Foundation (CSF) Institutional support MBU-M - RVO:61388971 UT WOS 000328179800042 DOI https://doi.org/10.1016/j.cellsig.2013.08.024 Annotation The ERR (extracellular signal-regulated kinases) cascade has an evolutionarily conserved three tier architecture consisting of protein kinases Raf, MEK (MAPK/ERK kinase) and ERK Following activation, ERK phosphorylates various cellular elements leading to diverse cellular responses. Downstream of ERK the family of p90 ribosomal 56 kinases (RSKs) has been proven to be an important conveyor of ERK signaling, however, little is known if ERK and RSK coordinate their functions to generate a specific biological response. Here we show that in epithelial cells conditional activation of the ERK pathway causes phenotypic conversion of epithelial cells to autonomously migrating cells, This process involves two sequential steps characterized by loss of apical-basal polarity followed by cell scattering. The activation of ERR, but not RSK, is sufficient for the execution of the first step and it requires calpain mediated remodeling of actin cytoskeleton. Conversely, RSK regulates the successive stage characterized by cell-cell contact weakening and increased cellular migration. Thus, ERK and RSK regulate different cellular subprograms and coordinated execution of these subprograms in time generates a relevant biological response. Our data also suggest that the mechanism by which the ERK pathway controls a cellular response may be distributed between ERK and RSK, rather than being elicited by a single effector kinase Workplace Institute of Microbiology Contact Eliška Spurná, eliska.spurna@biomed.cas.cz, Tel.: 241 062 231 Year of Publishing 2014
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