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Phosducin-like 3 (PDCL3); VEGF receptor 2 (KDR/Flk-1; VEGFR-2)

Cell culture studies suggest inhibiting PDCL3 could help treat VEGFR-2-dependent angiogenesis in tumors. In an aortic endothelial cell line, vector-mediated overexpression of PDCL3 increased VEGFR-2 stability and VEGFR-2-dependent capillary tube formation compared with wild-type PDCL3 expression. In a human umbilical vascular endothelial cell line, small interfering RNA-mediated knockdown of PDCL3 decreased VEGFR-2 protein levels and VEGF-dependent capillary tube formation compared with no knockdown. In human embryonic kidney cells, coexpression of VEGFR-2 and PDCL3 increased cell proliferation compared with expression of either protein alone. Next steps include conducting in vivo tests of PDCL3 function and developing small molecule inhibitors of PDCL3.

SciBX 6(29); doi:10.1038/scibx.2013.752
Published online Aug. 1, 2013

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Srinavasan, S. et al. J. Biol. Chem.; published online June 21, 2013;
Contact: Nader Rahimi, Boston University Medical Campus, Boston, Mass.