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    J Biol Chem. 2009 Oct 2;284(40):27409-15. Epub 2009 Aug 4.

    Suppression of tumor angiogenesis by Galpha(13) haploinsufficiency.

    Source

    Department of Physiology, Weill Medical College of Cornell University, New York, New York 10065, USA.

    Abstract

    Heterotrimeric G proteins are critical transducers of cellular signaling. Of the four families of G proteins, the physiological function of Galpha(13) is less well understood. Galpha(13) gene-deleted mice die at embryonic day approximately 9.5. Here, we show that heterozygous Galpha(13)(+/-) mice display defects in adult angiogenesis. Female Galpha(13)(+/-) mice showed a higher number of immature follicles and a lower density of blood vessels in the mature corpus luteum compared with Galpha(13)(+/+) mice. Furthermore, implanted tumors grew slower in Galpha(13)(+/-) host mice. These tumor tissues had many fewer blood vessels compared with those from Galpha(13)(+/+) host mice. Moreover, bone marrow-derived progenitor cells from Galpha(13)(+/+) mice rescued the failed growth of allografted tumors when reconstituted into irradiated Galpha(13)(+/-) mice. Hence, Galpha(13) is haploinsufficient for adult angiogenesis in both the female reproductive system and tumor angiogenesis.

    PMID:
    19654325
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2785670
    Free PMC Article

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