19 research outputs found

    The moderating role of emotion management in the relationship between mobbing and burnout

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    The purpose of the study was to investigate the moderating role of emotion management (emotion regulation and emotional intelligence) in the relationship between mobbing and burnout with two samples (220 nurses and 220 engineers). The reason to use two samples was to investigate and being consistent with the discussions that employees who have a non-service occupation might also experience burnout. In both samples, emotional intelligence moderated the relationship between mobbing and burnout but the effect was not in the hypothesized direction; it did not buffer the effects of mobbing on burnout. Furthermore, cognitive reappraisal which is the dimension of emotion regulation moderated the relationship between mobbing and reduced personal accomplishment/professional efficacy in both samples and cynicism in engineers but the effects were not in the hypothesized direction. Expressive suppression which is the other dimension of emotion regulation moderated the relationship between mobbing and reduced personal accomplishment/professional efficacy in both samples and cynicism in engineers.info:eu-repo/semantics/publishedVersio

    Functional divergence of the two Elongator subcomplexes during neurodevelopment

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    The highly conserved Elongator complex is a translational regulator that plays a critical role in neurodevelopment, neurological diseases, and brain tumors. Numerous clinically relevant variants have been reported in the catalytic Elp123 subcomplex, while no missense mutations in the accessory subcomplex Elp456 have been described. Here, we identify ELP4 and ELP6 variants in patients with developmental delay, epilepsy, intellectual disability, and motor dysfunction. We determine the structures of human and murine Elp456 subcomplexes and locate the mutated residues. We show that patient‐derived mutations in Elp456 affect the tRNA modification activity of Elongator in vitro as well as in human and murine cells. Modeling the pathogenic variants in mice recapitulates the clinical features of the patients and reveals neuropathology that differs from the one caused by previously characterized Elp123 mutations. Our study demonstrates a direct correlation between Elp4 and Elp6 mutations, reduced Elongator activity, and neurological defects. Foremost, our data indicate previously unrecognized differences of the Elp123 and Elp456 subcomplexes for individual tRNA species, in different cell types and in different key steps during the neurodevelopment of higher organisms
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