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Sox2 function as a negative regulator to control HAMP expression
Song, Bin; Bian, Qi; Shao, Cheng-Hao; Liu, An-An; Jing, Wei; Liu, Rui; Zhang, Yi-Jie; Zhou, Ying-Qi; Li, Gang; Jin, Gang.
  • Song, Bin; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Bian, Qi; Second Military Medical University. Changhai Hospital. Department of Nephrology. Shanghai. CN
  • Shao, Cheng-Hao; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Liu, An-An; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Jing, Wei; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Liu, Rui; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Zhang, Yi-Jie; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Zhou, Ying-Qi; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Li, Gang; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
  • Jin, Gang; Second Military Medical University. Changhai Hospital. Department of General Surgery. Shanghai. CN
Biol. Res ; 48: 1-8, 2015. graf
Artículo en Inglés | LILACS | ID: biblio-950787
ABSTRACT

BACKGROUND:

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.
Asunto(s)


Texto completo: Disponible Índice: LILACS (Américas) Asunto principal: Regulación Neoplásica de la Expresión Génica / Hepatocitos / Factores de Transcripción SOXB1 / Hepcidinas Tipo de estudio: Estudio pronóstico Límite: Humanos Idioma: Inglés Revista: Biol. Res Asunto de la revista: Biologia Año: 2015 Tipo del documento: Artículo País de afiliación: China Institución/País de afiliación: Second Military Medical University/CN

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Texto completo: Disponible Índice: LILACS (Américas) Asunto principal: Regulación Neoplásica de la Expresión Génica / Hepatocitos / Factores de Transcripción SOXB1 / Hepcidinas Tipo de estudio: Estudio pronóstico Límite: Humanos Idioma: Inglés Revista: Biol. Res Asunto de la revista: Biologia Año: 2015 Tipo del documento: Artículo País de afiliación: China Institución/País de afiliación: Second Military Medical University/CN