IndraLab
Statements
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"In the cell-free assay Li2CO3 significantly inhibited phosphoinositide 3-kinase (PI3K)-mediated phosphorylation of Akt1 at Ser473, but Li2CO3 did not affect PI3K-mediated PI(3,4,5)P3 production and 3-phosphoinositide-dependent protein kinase 1 (PDK1)-mediated phosphorylation of Akt1 at Thr308."
reach
"In general, receptor- or non-receptor tyrosine kinases, PI3K, the 3-phosphoinositide-dependent protein kinase 1 (PDK1) and mTOR complex 2 (mTORC2) can activate Akt by promoting the phosphorylation of Akt1, Akt2 and Akt3 at residues T308/S473, T309/S474 and T305/S472, respectively [83]."
reach
"PDK1 directly phosphorylates Akt1 at T308, while mTORC2 not only directly phosphorylates Akt1 at S473, but also phosphorylates and activates insulin receptor (InsR)/insulin-like growth factor receptor (IGF-IR) through the tyrosine kinase activity of mTOR, thereby indirectly promoting Akt activation [83, 85]."
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"Di-Poi et al. demonstrated this mechanism by elucidating that the proliferative effect of PPAR beta and delta was mediated through the direct repression of gene expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and increase expression of 3-phosphoinositide-dependent-protein kinase 1 (PDK1), which then activated the phosphorylation of protein kinase B (Akt), leading to cell proliferation of keratinocytes [XREF_BIBR]."
reach
"In general, receptor- or non-receptor tyrosine kinases, PI3K, the 3-phosphoinositide-dependent protein kinase 1 (PDK1) and mTOR complex 2 (mTORC2) can activate Akt by promoting the phosphorylation of Akt1, Akt2 and Akt3 at residues T308/S473, T309/S474 and T305/S472, respectively [83]."