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dc.contributor.authorPan, Dongning
dc.contributor.authorMao, Chunxiao
dc.contributor.authorWang, Yong-Xu
dc.date2022-08-11T08:10:15.000
dc.date.accessioned2022-08-23T17:01:27Z
dc.date.available2022-08-23T17:01:27Z
dc.date.issued2013-06-05
dc.date.submitted2013-07-25
dc.identifier.citationPLoS One. 2013 Jun 5;8(6):e66294. doi: 10.1371/journal.pone.0066294. Print 2013. <a href="http://dx.doi.org/10.1371/journal.pone.0066294">Link to article on publisher's site</a>
dc.identifier.issn1932-6203 (Linking)
dc.identifier.doi10.1371/journal.pone.0066294
dc.identifier.pmid23755305
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44011
dc.description.abstractAberrant gluconeogenic gene expression is associated with diabetes, glycogen storage disease, and liver cancer. However, little is known how these genes are regulated at the chromatin level. In this study, we investigated in HepG2 cells whether histone demethylation is a potential mechanism. We found that knockdown or pharmacological inhibition of histone demethylase LSD1 causes remarkable transcription activation of two gluconeogenic genes, FBP1 and G6Pase, and consequently leads to increased de novo glucose synthesis and decreased intracellular glycogen content. Mechanistically, LSD1 occupies the promoters of FBP1 and G6Pase, and modulates their H3K4 dimethylation levels. Thus, our work identifies an epigenetic pathway directly governing gluconeogenic gene expression, which might have important implications in metabolic physiology and diseases.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23755305&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>Copyright: © 2013 Pan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</p>
dc.subjectGene Expression Regulation
dc.subjectHep G2 Cells
dc.subjectHistone Demethylases
dc.subjectGenetics and Genomics
dc.subjectMolecular Biology
dc.subjectMolecular Genetics
dc.titleSuppression of Gluconeogenic Gene Expression by LSD1-Mediated Histone Demethylation
dc.typeArticle
dc.source.journaltitlePloS one
dc.source.volume8
dc.source.issue6
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1218&amp;context=pgfe_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pgfe_pp/218
dc.identifier.contextkey4349868
refterms.dateFOA2022-08-23T17:01:27Z
html.description.abstract<p>Aberrant gluconeogenic gene expression is associated with diabetes, glycogen storage disease, and liver cancer. However, little is known how these genes are regulated at the chromatin level. In this study, we investigated in HepG2 cells whether histone demethylation is a potential mechanism. We found that knockdown or pharmacological inhibition of histone demethylase LSD1 causes remarkable transcription activation of two gluconeogenic genes, FBP1 and G6Pase, and consequently leads to increased de novo glucose synthesis and decreased intracellular glycogen content. Mechanistically, LSD1 occupies the promoters of FBP1 and G6Pase, and modulates their H3K4 dimethylation levels. Thus, our work identifies an epigenetic pathway directly governing gluconeogenic gene expression, which might have important implications in metabolic physiology and diseases.</p>
dc.identifier.submissionpathpgfe_pp/218
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentProgram in Gene Function and Expression
dc.source.pagese66294


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