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Sox2 function as a negative regulator to control HAMP expression.

AbstractBACKGROUND:
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, it is an important 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.
AuthorsBin Song, Qi Bian, Cheng-Hao Shao, An-An Liu, Wei Jing, Rui Liu, Yi-Jie Zhang, Ying-Qi Zhou, Gang Li, Gang Jin
JournalBiological research (Biol Res) Vol. 48 Pg. 23 (May 06 2015) ISSN: 0717-6287 [Electronic] England
PMID25943891 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • BMP2 protein, human
  • Bone Morphogenetic Protein 2
  • HAMP protein, human
  • Hepcidins
  • Interleukin-6
  • SOX2 protein, human
  • SOXB1 Transcription Factors
  • Iron
  • Luciferases
Topics
  • Anemia (genetics, metabolism)
  • Binding Sites
  • Bone Morphogenetic Protein 2 (metabolism)
  • Gene Expression Regulation, Neoplastic (genetics)
  • Gene Knockdown Techniques
  • Genetic Vectors
  • Hep G2 Cells
  • Hepatocytes (metabolism)
  • Hepcidins (genetics, metabolism)
  • Humans
  • Interleukin-6 (metabolism)
  • Iron (metabolism)
  • Luciferases
  • Plasmids (genetics)
  • Promoter Regions, Genetic (genetics)
  • SOXB1 Transcription Factors (genetics, metabolism)

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