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        Attitudes and opinions regarding leadership qualities of marketing executives: A quantitative analysis

        Myles Bassell,Sonia Lambert,Hershey H. Friedman 한국마케팅과학회 2019 마케팅과학연구 Vol.29 No.1

        In this research study, students at a large urban university completed our questionnaire regarding leadership. The student’s opinions regarding leadership qualities are consistent with our literature review. Marketing leaders need to be creative, global thinkers, with integrity who can create innovative learning organizations, encourage diversity, and ensure employees are engaged in meaningful work that achieves sustainability and results in a competitive advantage.

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        Upf1 Phosphorylation Triggers Translational Repression during Nonsense-Mediated mRNA Decay

        Isken, Olaf,Kim, Yoon Ki,Hosoda, Nao,Mayeur, Greg L.,Hershey, John W.B.,Maquat, Lynne E. Elsevier 2008 Cell Vol.133 No.2

        <P><B>Summary</B></P><P>In mammalian cells, nonsense-mediated mRNA decay (NMD) generally requires that translation terminates sufficiently upstream of a post-splicing exon junction complex (EJC) during a pioneer round of translation. The subsequent binding of Upf1 to the EJC triggers Upf1 phosphorylation. We provide evidence that phospho-Upf1 functions after nonsense codon recognition during steps that involve the translation initiation factor eIF3 and mRNA decay factors. Phospho-Upf1 interacts directly with eIF3 and inhibits the eIF3-dependent conversion of 40S/Met-tRNA<SUB>i</SUB><SUP>Met</SUP>/mRNA to translationally competent 80S/Met-tRNA<SUB>i</SUB><SUP>Met</SUP>/mRNA initiation complexes to repress continued translation initiation. Consistent with phospho-Upf1 impairing eIF3 function, NMD fails to detectably target nonsense-containing transcripts that initiate translation independently of eIF3 from the CrPV IRES. There is growing evidence that translational repression is a key transition that precedes mRNA delivery to the degradation machinery. Our results uncover a critical step during NMD that converts a pioneer translation initiation complex to a translationally compromised mRNP.</P>

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