Thank You South Korea! CXXC5 is a transcriptional activator of Flk-1 and mediates bone morphogenic protein-induced endothelial cell differentiation and vessel formation. ncbi.nlm.nih.gov/pubmed/24136587 FASEB J. 2013 Oct 17. [Epub ahead of print] Kim HY, Yang DH, Shin SW, Kim MY, Yoon JH, Kim S, Park HC, Kang DW, Min D, Hur MW, Choi KY. Source *Translational Research Center for Protein Function Control, †Department of Biotechnology, College of Life Science and Biotechnology, and ‡Department of Biochemistry and Molecular Biology, College of Medicine, Yonsei University, Seoul, South Korea; Abstract CXXC5 is a member of a small subset of proteins containing CXXC-type zinc-finger domain. Here, we show that CXXC5 is a transcription factor activating Flk-1, a receptor for vascular endothelial growth factor. CXXC5 and Flk-1 were accmulated in nucli and membrane of mouse embryonic stem cells (mESCs), respectively, during their endothelial differentiation. CXXC5 overexpression induced Flk-1 transcription in both endothelium-differentiated mESCs and human umbilical vein endothelial cells (HUVECs). In vitro DNA binding assay showed direct interaction of CXXC5 on the Flk-1 promoter region, and mutation on its DNA-binding motif abolished transcriptional activity. We showed that bone morphorgeneic protein 4 (BMP4) induced CXXC5 transcription in the cells, and inhibitors of BMP signaling suppressed the CXXC5 induction and the consequent Flk-1 induction by BMP4 treatment. CXXC5 knockdown resulted in suppression of BMP4-induced stress fiber formation (56.8±1.3% decrease, P
Posted on: Wed, 23 Oct 2013 13:32:43 +0000
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