IndraLab

Statements


Phosphorylated MTOR phosphorylates RPS6KB1. 9 / 9
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"We reported that IPostC increases phosphorylated Akt (p-Akt), phosphorylated mTOR (p-mTOR), phosphorylated S6K (p-S6K), and phosphorylated 4EBP1 (p-4EBP1) in the mTOR pathway and increases the presynaptic growth associated protein 43 (GAP43) protein levels (Xie et al., 2013)."

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"MTOR phosphorylation led to the phosphorylation of p70S6K, mTOR dependent event, that was abrogated by the mTOR specific inhibitor rapamycin."

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"In general, p-mTOR induces phosphorylation of 4E-BP1 and P70S6K, and initiation of translation and protein synthesis."

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"Because of the apparently discordant results noted above related to mTOR kinase activation (e.g., no change in mTOR and 4E-BP1 phosphorylation, but increased S6K1 phosphorylation), we also assessed key up-stream regulators of mTOR activity."

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"In the downstream mTOR signaling pathways, p-mTOR can improve the translation efficiency of 5 '-TOR mRNA and accelerate protein synthesis by phosphorylating its downstream receptors during the translation process, such as elF4E and p70S6 kinase [XREF_BIBR]."

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"The expression of p-mTOR, mTOR-mediated phosphorylation of p70 ribosomal S6 protein kinase 1 (p-S6K1), 4 E-binding protein 4 (p-4 E-BP1), as well as phosphatidylinositide 3-kinase (p-PI3K) pathway were amplified in cyclophosphamide rats as compared with control rats."

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"We reported that IPostC increases phosphorylated Akt (p-Akt), phosphorylated mTOR (p-mTOR), phosphorylated S6K (p-S6K), and phosphorylated 4EBP1 (p-4EBP1) in the mTOR pathway and increases the presynaptic growth associated protein 43 (GAP43) protein levels (Xie et al., 2013)."

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"The p-mTOR activates p70S6K, and phosphorylated p70S6K combines with translation initiation complexes, to improve the efficiency of mRNA translation [XREF_BIBR]."

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"Critical components in the translational machinery, such as phosphorylated mammalian target of rapamycin (mTOR) and its downstream targets, phosphorylated eukaryotic translation initiation factor and p70 S6 kinase, were up-regulated following NO treatment, and inhibition of mTOR with rapamycin attenuated NO induced increase of cyclin D1 and ODC."