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Provedor de dados:  Genet. Mol. Biol.
País:  Brazil
Título:  Six1 induces protein synthesis signaling expression in duck myoblasts mainly via up-regulation of mTOR
Autores:  Wang,Haohan
Li,Xinxin
Liu,Hehe
Sun,Lingli
Zhang,Rongping
Li,Liang
Wangding,Mincheng
Wang,Jiwen
Data:  2016-03-01
Ano:  2016
Palavras-chave:  Duck
Six1
Protein metabolism signaling
MTOR
PEGFP-duSix1
Resumo:  Abstract As a critical transcription factor, Six1 plays an important role in the regulation of myogenesis and muscle development. However, little is known about its regulatory mechanism associated with muscular protein synthesis. The objective of this study was to investigate the effects of overexpression ofSix1 on the expression of key protein metabolism-related genes in duck myoblasts. Through an experimental model where duck myoblasts were transfected with a pEGFP-duSix1 construct, we found that overexpression of duckSix1 could enhance cell proliferation activity and increase mRNA expression levels of key genes involved in the PI3K/Akt/mTOR signaling pathway, while the expression of FOXO1, MuRF1and MAFbx was not significantly altered, indicating thatSix1 could promote protein synthesis in myoblasts through up-regulating the expression of several related genes. Additionally, in duck myoblasts treated with LY294002 and rapamycin, the specific inhibitors ofPI3K and mTOR, respectively, the overexpression of Six1 could significantly ameliorate inhibitive effects of these inhibitors on protein synthesis. Especially, the mRNA expression levels of mTOR and S6K1 were observed to undergo a visible change, and a significant increase in protein expression of S6K1 was seen. These data suggested that Six1plays an important role in protein synthesis, which may be mainly due to activation of the mTOR signaling pathway.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572016000100151
Editor:  Sociedade Brasileira de Genética
Relação:  10.1590/1678-4685-GMB-2015-0075
Formato:  text/html
Fonte:  Genetics and Molecular Biology v.39 n.1 2016
Direitos:  info:eu-repo/semantics/openAccess
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