http://www.cnr.it/ontology/cnr/individuo/prodotto/ID180350
3,5,3'triiodo-L-thyronine induces SREBP-1 expression by non-genomic actions in human Hep G2 cells (Articolo in rivista)
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- 3,5,3'triiodo-L-thyronine induces SREBP-1 expression by non-genomic actions in human Hep G2 cells (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1002/jcp.22974 (literal)
- Alternative label
Gnoni GV; Rochira A, Leone A, Damiano F, Marsiliante S, Siculella L (2012)
3,5,3'triiodo-L-thyronine induces SREBP-1 expression by non-genomic actions in human Hep G2 cells
in Journal of cellular physiology (Online); John Wiley & Sons Ltd., Chichester (Regno Unito)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Gnoni GV; Rochira A, Leone A, Damiano F, Marsiliante S, Siculella L (literal)
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- http://onlinelibrary.wiley.com/store/10.1002/jcp.22974/asset/22974_ftp.pdf?v=1&t=h1erc55r&s=6e67d6ca1f8a946a55d05a15ffd4d8c8db647370 (literal)
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- Laboratory of Biochemistry and Molecular Biology, Department of Biological and Environmental Sciences and Technologies,
University of Salento, Via Prov.le Lecce-Monteroni, Lecce, Italy;
National Research Council, Institute of Science of Food Production (CNR, ISPA), Lecce, Italy;
Laboratory of Cellular Physiology, Department of Biological and Environmental Sciences and Technologies, University of Salento,
Via Prov.le Lecce-Monteroni, Lecce, Italy; (literal)
- Titolo
- 3,5,3'triiodo-L-thyronine induces SREBP-1 expression by non-genomic actions in human Hep G2 cells (literal)
- Abstract
- Liver is an important target for thyroid hormone actions. T3 exerts its effects by two mechanisms: (i) Genomic actions consisting of T3 link
to nuclear receptors that bind responsive elements in the promoter of target genes, (ii) non-genomic actions including integrin avb3
receptor-mediated MAPK/ERK and PI3K/Akt/mTOR-C1 activation. SREBP-1a, SREBP-1c, and SREBP-2 are transcription factors involved
in the regulation of lipogenic genes. We show in Hep G2 cells that T3 determined a dose- and time-dependent increase in the level of the
precursor form of SREBP-1 without affecting SREBP-1 mRNA abundance. T3 also induced phosphorylation of ERK1/2, Akt and of mTORC1
target S6K-P70, and the cytosol-to-membrane translocation of PKC-a. Modulation of SREBP-1 protein level by T3 was dependent on
MAPK/ERK, PI3K/Akt/mTOR-C1 pathway activation since the MEK inhibitor PD98059 or the PI3K inhibitor LY294002 abolished the
stimulatory effect of T3. Conversely, the effect of T3 on SREBP-1 level was enhanced by using rapamycin, mTOR-C1 inhibitor. These data
suggest a negative control of mTOR-C1 target S6K-P70 on PI3K/Akt pathway. The effect of T3 on SREBP-1 content increased also by using
PKC inhibitors. These inhibitors increased the action of T3 on Akt phosphorylation suggesting that conventional PKCs may work as
negative regulators of the T3-dependent SREBP-1 increase. T3 effects were partially abrogated by tetrac, an inhibitor of the T3-avb3
receptor interaction and partially evoked by T3 analog T3-agarose. These findings support a model in which T3 activates intracellular
signaling pathways which may be involved in the increment of SREBP-1 level through an IRES-mediated translation mechanism.
J. Cell. Physiol. 227: 2388-2397, 2012. (literal)
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