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dc.creatorSong,Bin
dc.creatorBian,Qi
dc.creatorShao,Cheng-Hao
dc.creatorLiu,An-An
dc.creatorJing,Wei
dc.creatorLiu,Rui
dc.creatorZhang,Yi-Jie
dc.creatorZhou,Ying-Qi
dc.creatorLi,Gang
dc.creatorJin,Gang
dc.date2015-01-01
dc.date.accessioned2019-05-02T21:22:26Z
dc.date.available2019-05-02T21:22:26Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602015000100023
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/82513
dc.descriptionBACKGROUND: Hepcidin, encoding by HAMP gene, is the pivotal regulator of iron metabolism, controlling the systemic absorption and transportation of irons from intracellular stores. Abnormal levels of HAMP expression alter plasma iron parameters and lead to iron metabolism disorders. Therefore,itis animportant goal to understand the mechanisms controlling HAMP gene expression. RESULTS: Overexpression of Sox2 decrease basal expression of HAMP or induced by IL-6 or BMP-2, whereas, knockdown of Sox2 can increase HAMP expression, furthermore, two potential Sox2-binding sites were identified within the human HAMP promoter. Indeed, luciferase experiments demonstrated that deletion of any Sox2-binding site impaired the negative regulation of Sox2 on HAMP promoter transcriptional activity in basal conditions. ChIP experiments showed that Sox2 could directly bind to these sites. Finally, we verified the role of Sox2 to negatively regulate HAMP expression in human primary hepatocytes. CONCLUSION: We found that Sox2 as a novel factor to bind with HAMP promoter to negatively regulate HAMP expression, which may be further implicated as a therapeutic option for the amelioration of HAMP-overexpression-related diseases, including iron deficiency anemia.
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dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.1186/s40659-015-0013-z
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.48 2015
dc.subjectSox2
dc.subjectGene expression
dc.subjectHepatocyte
dc.subjectHAMP
dc.subjectIron metabolism
dc.titleSox2 function as a negative regulator to control HAMP expression


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