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Vijayaraj, Preethi

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Vijayaraj

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Preethi

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Vijayaraj, Preethi

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    ERG is Required for the Differentiation of Embryonic Stem Cells along the Endothelial Lineage
    (BioMed Central, 2009) Nikolova-Krstevski, Vesna; Yuan, Lei; Le Bras, Alexandra; Vijayaraj, Preethi; Kondo, Maiko; Gebauer, Marie-Isabel; Bhasin, Manoj; Carman, Christopher; Oettgen, Peter
    Background: The molecular mechanisms that govern stem cell differentiation along the endothelial lineage remain largely unknown. Ets related gene (ERG) has recently been shown to participate in the transcriptional regulation of a number of endothelial specific genes including VE-cadherin (CD144), endoglin, and von Willebrand's Factor (vWF). The specific role of the ETS factor ERG during endothelial differentiation has not been evaluated. Results: ERG expression and function were evaluated during the differentiation of embryonic stem cells into embryoid bodies (EB). The results of our study demonstrate that ERG is first expressed in a subpopulation of vascular endothelial growth factor receptor 2 (VEGF-R2) expressing cells that also express VE-cadherin. During ES cell differentiation, ERG expression remains restricted to cells of the endothelial lineage that eventually coalesce into primitive vascular structures within embryoid bodies. ERG also exhibits an endothelial cell (EC)-restricted pattern during embryogenesis. To further define the role of ERG during ES cell differentiation, we used a knockdown strategy to inhibit ERG expression. Delivery of three independent shRNA led to 70-85% reductions in ERG expression during ES cell differentiation compared to no change with control shRNA. ERG knockdown was associated with a marked reduction in the number of ECs, the expression of EC-restricted genes, and the formation of vascular structures. Conclusion: The ETS factor ERG appears to be a critical regulator of EC differentiation.
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    Keratins Regulate Protein Biosynthesis Through Localization of GLUT1 and -3 Upstream of AMP Kinase and Raptor
    (The Rockefeller University Press, 2009) Vijayaraj, Preethi; Kröger, Cornelia; Reuter, Ursula; Windoffer, Reinhard; Leube, Rudolf E.; Magin, Thomas M.
    Keratin intermediate filament proteins form cytoskeletal scaffolds in epithelia, the disruption of which affects cytoarchitecture, cell growth, survival, and organelle transport. However, owing to redundancy, the global function of keratins has not been defined in full. Using a targeted gene deletion strategy, we generated transgenic mice lacking the entire keratin multiprotein family. In this study, we report that without keratins, embryonic epithelia suffer no cytolysis and maintain apical polarity but display mislocalized desmosomes. All keratin­null embryos die from severe growth retardation at embryonic day 9.5. We find that GLUT1 and ­3 are mislocalized from the apical plasma membrane in embryonic epithelia, which subsequently activates the energy sensor adenosine monophosphate kinase (AMPK). Analysis of the mammalian target of rapamycin (mTOR) pathway reveals that AMPK induction activates Raptor, repressing protein biosynthesis through mTORC1’s downstream targets S6 kinase and 4E­binding protein 1. Our findings demonstrate a novel keratin function upstream of mTOR signaling via GLUT localization and have implications for pathomechanisms and therapy approaches for keratin disorders and the analysis of other gene families.