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• W2019904955 abstract "Runx transcription factors regulate viral growth, hematopoiesis, bone formation, angiogenesis, and gastric epithelial development through specific DNA-binding motifs on target gene promoters. Vascular endothelial cells (ECs) express RUNX genes that are activated by angiogenic factors. The RUNX2 gene also activates the vascular endothelial growth factor promoter. Alternatively spliced forms of RUNX genes have been described, but their functions in angiogenesis have not been elucidated. In this study, expression of a novel alternatively spliced variant of RUNX2 (RUNX2Δ8), lacking the region encoded by exon 8, was detected in aortic tissue undergoing angiogenesis in vitro and in ECs. Expression of RUNX2 and RUNX2Δ8 increased in vascular sprouts concomitant with expression of cellular proteases and cytokines known to mediate angiogenesis. RUNX2 DNA-binding activity was expressed in proliferating but not quiescent ECs. Ectopic expression of RUNX2 in ECs increased cell sprouting, cell proliferation, DNA synthesis, and phosphorylation of phosphorylated retinoblastoma relative to control transfectants while RUNX2, but not RUNX2Δ8 transfectants, acquired resistance to growth inhibition by transforming growth factor (TGFβ1). Furthermore, RUNX2Δ8-transfected cells were more sensitive to TGFβ1-induced apoptosis than RUNX2 transfectants. Consistent with these data, the RUNX2 gene was a strong repressor of the promoter of the cyclin-dependent kinase inhibitor, p21CIP1, while RUNX2Δ8 was a competitive inhibitor of RUNX2 and exhibited weak repression activity. These results support the hypothesis that ECs regulate growth and apoptosis, in part, by alternative splicing events in the RUNX2 transcription factor to affect the TGFβ1 signaling pathway. The exon 8 domain of RUNX2 may contribute to the strong repression activity of RUNX2 for some target gene promoters." @default.
• W2019904955 created "2016-06-24" @default.
• W2019904955 creator A5006613618 @default.
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• W2019904955 date "2004-04-26" @default.
• W2019904955 modified "2023-10-10" @default.
• W2019904955 title "Regulation of TGFβ1-mediated growth inhibition and apoptosis by RUNX2 isoforms in endothelial cells" @default.
• W2019904955 cites W1525835719 @default.
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• W2019904955 cites W1596240955 @default.
• W2019904955 cites W1796060835 @default.
• W2019904955 cites W1890692607 @default.
• W2019904955 cites W1963793607 @default.
• W2019904955 cites W1964702114 @default.
• W2019904955 cites W1966968552 @default.
• W2019904955 cites W1967948255 @default.
• W2019904955 cites W1971353320 @default.
• W2019904955 cites W1971613536 @default.
• W2019904955 cites W1972705953 @default.
• W2019904955 cites W1973023394 @default.
• W2019904955 cites W1973047647 @default.
• W2019904955 cites W1973630430 @default.
• W2019904955 cites W1975573720 @default.
• W2019904955 cites W1985197859 @default.
• W2019904955 cites W1992184028 @default.
• W2019904955 cites W1994596418 @default.
• W2019904955 cites W1996474776 @default.
• W2019904955 cites W1997812904 @default.
• W2019904955 cites W1998770945 @default.
• W2019904955 cites W2000000541 @default.
• W2019904955 cites W2003617876 @default.
• W2019904955 cites W2011745548 @default.
• W2019904955 cites W2015519364 @default.
• W2019904955 cites W2016068460 @default.
• W2019904955 cites W2025046506 @default.
• W2019904955 cites W2036817346 @default.
• W2019904955 cites W2041279982 @default.
• W2019904955 cites W2043558120 @default.
• W2019904955 cites W2050039508 @default.
• W2019904955 cites W2058139610 @default.
• W2019904955 cites W2059029313 @default.
• W2019904955 cites W2059556382 @default.
• W2019904955 cites W2065340005 @default.
• W2019904955 cites W2067786908 @default.
• W2019904955 cites W2068120597 @default.
• W2019904955 cites W2072088194 @default.
• W2019904955 cites W2075559846 @default.
• W2019904955 cites W2079985291 @default.
• W2019904955 cites W2080598876 @default.
• W2019904955 cites W2083319499 @default.
• W2019904955 cites W2085061661 @default.
• W2019904955 cites W2085823469 @default.
• W2019904955 cites W2085896636 @default.
• W2019904955 cites W2086447178 @default.
• W2019904955 cites W2091851050 @default.
• W2019904955 cites W2093820637 @default.
• W2019904955 cites W2094237675 @default.
• W2019904955 cites W2098305726 @default.
• W2019904955 cites W2099985524 @default.
• W2019904955 cites W2107964792 @default.
• W2019904955 cites W2116217777 @default.
• W2019904955 cites W2119824866 @default.
• W2019904955 cites W2125946663 @default.
• W2019904955 cites W2133193835 @default.
• W2019904955 cites W2136530946 @default.
• W2019904955 cites W2150048971 @default.
• W2019904955 cites W2152215024 @default.
• W2019904955 cites W2159779481 @default.
• W2019904955 cites W2171597870 @default.
• W2019904955 cites W2171767704 @default.
• W2019904955 cites W2317319369 @default.
• W2019904955 cites W2330795003 @default.
• W2019904955 cites W4230622630 @default.
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• W2019904955 cites W4249388929 @default.
• W2019904955 cites W4249587222 @default.
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• W2019904955 doi "https://doi.org/10.1038/sj.onc.1207589" @default.
• W2019904955 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15107836" @default.
• W2019904955 hasPublicationYear "2004" @default.
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