Gonadotropin releasing hormone activation of the mTORC2/Rictor complex regulates actin remodeling and ERK activity in LßT2 cells.
Mol Cell Endocrinol
; 439: 346-353, 2017 01 05.
Article
em En
| MEDLINE
| ID: mdl-27663077
ABSTRACT
The mammalian target of rapamycin (mTOR) assembles into two different multi-protein complexes, mTORC1 and mTORC2. The mTORC2 complex is distinct due to the unique expression of the specific core regulatory protein Rictor (rapamycin-insensitive companion of mTOR). mTORC2 has been implicated in regulating actin cytoskeletal reorganization but its role in gonadotrope function is unknown. Using the gonadotrope-derived LßT2 cell line, we find that the GnRH agonist buserelin (GnRHa) phosphorylates both mTOR and Rictor. Interestingly, inhibition of mTORC2 blunts GnRHa-induced cyto-architectural rearrangements. Coincident with blunting of actin reorganization, inhibition of mTORC2 also attenuates GnRHa-mediated activation of both protein kinase C (PKC) and extracellular signal regulated kinase (ERK). Collectively, our data suggests that GnRHa-mediated mTORC2 activation is important in facilitating actin reorganization events critical for initiating PKC activity and subsequent ERK phosphorylation in the gonadotrope-derived LßT2 cell line.
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MEDLINE
Assunto principal:
Proteínas de Transporte
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Hormônio Liberador de Gonadotropina
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Actinas
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MAP Quinases Reguladas por Sinal Extracelular
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Gonadotrofos
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Alvo Mecanístico do Complexo 2 de Rapamicina
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article