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Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells.

Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells. Research Abstract Details 

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  • Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells. Abstract Text:

    yun luYun Lu,j michael thomsonJ Michael Thomson,ho yuen frank wongHo Yuen Frank Wong,scott m hammondScott M Hammond,brigid l m hoganBrigid L M Hogan,yun luYun Lu,j michael thomsonJ Michael Thomson,ho yuen frank wongHo Yuen Frank Wong,scott m hammondScott M Hammond,brigid l m hoganBrigid L M Hogan,

    The miR-17-92 locus encodes a cluster of 7 microRNAs transcribed as a single primary transcript. It can accelerate c-Myc induced B cell lymphoma development and is highly expressed in many tumors, including lung tumors. However, the role of miR-17-92 in development has not been well studied. From analysis of microRNAs during lung development, expression of the miR-17-92 cluster is high at early stages, but declines as development proceeds. We used the mouse surfactant protein C (Sftpc) promoter to over-express the cluster in embryonic lung epithelium. Transgenic lungs have a very abnormal lethal phenotype. They contain numerous proliferative epithelial cells that retain high levels of Sox9, a marker of distal progenitors. The differentiation of proximal epithelial cells was also inhibited. Furthermore, a significant increase in the number of neuroendocrine cell clusters was observed in the lungs of dead transgenic pups. We identify a tumor suppressor, Rbl2 which belongs to the Rb family, as a new target for miR-17-5p. Together, these studies suggest that mir-17-92 normally promotes the high proliferation and undifferentiated phenotype of lung epithelial progenitor cells.

    Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells. Publishing Authors By Initials

    y luY Lu,jm thomsonJM Thomson,hy wongHY Wong,sm hammondSM Hammond,bl hoganBL Hogan,y luY Lu,jm thomsonJM Thomson,hy wongHY Wong,sm hammondSM Hammond,bl hoganBL Hogan,

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    Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Developmental biology

    VOLUME: 310

    Page Numbers: 442-53

    Journal Abbreviation: Dev. Biol.

    ISSN: 0012-1606

    DAY: 9

    MONTH: 08

    YEAR: 2007

    Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells. Information

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    LANGUAGE: eng

    NlmUniqueID: 372762

    Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells. Keywords Mesh Terms:

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    Grant and Affiliation Information for Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells.

    AFFILIATION: Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: R01 HL071303-15

    ACRONYM: HL

    MEDLINETA: Dev Biol

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