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作者Gu, S.H.;Hsieh, Y.C.;Lin, P.L.
出版日期2017
著作名稱Signaling involved in PTTH-stimulated 4E-BP phosphorylation in prothoracic gland cells of Bombyx mori
刊名Journal of Insect Physiology
96
頁數1-8
被收錄索引SCI
關鍵字4E-BP; AMPK; Ecdysone; Prothoracic gland; Signal transduction
摘要Our previous studies showed that adenosine 5’-monophosphate-activated protein kinase (AMPK)/the target of rapamycin (TOR) signaling is involved in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis in Bombyx mori prothoracic glands (PGs). In the present study, we further investigated the signaling involved in PTTH-stimulated phosphorylation of 4E-BP. We found that 4E-BP phosphorylation stimulated by PTTH was partially reduced in Ca2 -free medium, indicating the involvement of Ca2 . In addition, we found that a potent and specific inhibitor of phospholipase C (PLC), U73122, greatly inhibited 4E-BP phosphorylation. However, PTTH-stimulated 4E-BP phosphorylation was not attenuated by a protein kinase C (PKC) inhibitor (chelerythrine C). These results indicate that PLC, but not PKC, is involved in PTTH-stimulated 4E-BP phosphorylation. When PGs were treated with agents that directly elevate the intracellular Ca2 concentration (either A23187 or thapsigargin), a great increase in 4E-BP phosphorylation was observed. A23187-stimulated phosphorylation of 4E-BP was partially blocked by a chemical activator of AMPK (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside, AICAR) and a phosphoinositide 3-kinase (PI3K) inhibitor (LY294002), but not by U0126, indicating involvement of AMPK and PI3K. Determination of AMPK phosphorylation showed that treatment with either A23187 or thapsigargin inhibited AMPK phosphorylation. Moreover, PTTH appeared to inhibit AMPK phosphorylation in a Ca2 -dependent manner. Altogether, these results indicate interconnections among Ca2 signaling, AMPK, and 4E-BP phosphorylation in PTTH-activated PGs of B. mori.
DOI10.1016/j.jinsphys.2016.10.007
系統號NO000004106

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