Matches in Nanopublications for { ?s ?p "[These findings strongly suggest that epigenetic dysregulation involving interactions between histone deacetylation and hypermethylation is responsible for targeted repression of IP-10 and potentially other antifibrotic genes in fibrotic lung disease and that this is amenable to therapeutic targeting.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ?g. }
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- NP909545.RA-9JjYfFFBuEFA-3q1dgwL2R0HC2u3pigg1JD15oOFUc130_assertion description "[These findings strongly suggest that epigenetic dysregulation involving interactions between histone deacetylation and hypermethylation is responsible for targeted repression of IP-10 and potentially other antifibrotic genes in fibrotic lung disease and that this is amenable to therapeutic targeting.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP909545.RA-9JjYfFFBuEFA-3q1dgwL2R0HC2u3pigg1JD15oOFUc130_provenance.
- assertion description "[These findings strongly suggest that epigenetic dysregulation involving interactions between histone deacetylation and hypermethylation is responsible for targeted repression of IP-10 and potentially other antifibrotic genes in fibrotic lung disease and that this is amenable to therapeutic targeting.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
- NP806978.RAVI0KU90iZuySuKpGMhLe7WfHkb-NhZadJas2QfVpFJk130_assertion description "[These findings strongly suggest that epigenetic dysregulation involving interactions between histone deacetylation and hypermethylation is responsible for targeted repression of IP-10 and potentially other antifibrotic genes in fibrotic lung disease and that this is amenable to therapeutic targeting.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP806978.RAVI0KU90iZuySuKpGMhLe7WfHkb-NhZadJas2QfVpFJk130_provenance.
- NP510182.RAl8rNEvqOQXUYKmFSUxrfPXW_teT654Tb9E1fAhOd7JM130_assertion description "[These findings strongly suggest that epigenetic dysregulation involving interactions between histone deacetylation and hypermethylation is responsible for targeted repression of IP-10 and potentially other antifibrotic genes in fibrotic lung disease and that this is amenable to therapeutic targeting.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP510182.RAl8rNEvqOQXUYKmFSUxrfPXW_teT654Tb9E1fAhOd7JM130_provenance.