Matches in SemOpenAlex for { <https://semopenalex.org/work/W2912244582> ?p ?o ?g. }
- W2912244582 abstract "In an effort to identify human endothelial cell (EC)-enriched lncRNAs,~500 lncRNAs were shown to be highly restricted in primary human ECs. Among them, lncEGFL7OS, located in the opposite strand of the EGFL7/miR-126 gene, is regulated by ETS factors through a bidirectional promoter in ECs. It is enriched in highly vascularized human tissues, and upregulated in the hearts of dilated cardiomyopathy patients. LncEGFL7OS silencing impairs angiogenesis as shown by EC/fibroblast co-culture, in vitro/in vivo and ex vivo human choroid sprouting angiogenesis assays, while lncEGFL7OS overexpression has the opposite function. Mechanistically, lncEGFL7OS is required for MAPK and AKT pathway activation by regulating EGFL7/miR-126 expression. MAX protein was identified as a lncEGFL7OS-interacting protein that functions to regulate histone acetylation in the EGFL7/miR-126 promoter/enhancer. CRISPR-mediated targeting of EGLF7/miR-126/lncEGFL7OS locus inhibits angiogenesis, inciting therapeutic potential of targeting this locus. Our study establishes lncEGFL7OS as a human/primate-specific EC-restricted lncRNA critical for human angiogenesis." @default.
- W2912244582 created "2019-02-21" @default.
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- W2912244582 date "2019-02-11" @default.
- W2912244582 modified "2023-09-30" @default.
- W2912244582 title "LncEGFL7OS regulates human angiogenesis by interacting with MAX at the EGFL7/miR-126 locus" @default.
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- W2912244582 doi "https://doi.org/10.7554/elife.40470" @default.
- W2912244582 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6370342" @default.
- W2912244582 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30741632" @default.
- W2912244582 hasPublicationYear "2019" @default.
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