IndraLab
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"For example, activated AKT can directly phosphorylate GSK3 to inhibit its activity XREF_BIBR; this leads to the nuclear translocation of beta-catenin to induce the expression of several cell cycle related genes such as CCND1 (symbol of Cyclin D1), which then promotes cell cycle progression via regulation of Rb phosphorylation."
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"We found FGF1 binds to the FGFR, resulting in the phosphorylation of Akt, which in turn phosphorylates GSK3β at Ser9, rendering the kinase-inactive and resulting in decreased phosphorylation of downstream substrates, including β-catenin.Although Tian-Song Liang has found that MicroRNA-506 can inhibit NPC tumour growth and metastasis by downregulating LHX2 [44], our study further extended the downstream targets and signalling pathway by which LHX2 serve as the oncogene in NPC, providing potential therapeutic strategies, such as FGF1/FGFR inhibitors."
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"For instance, two pancreatic cancer cell lines, PANC1 and ASPC1, exhibit amplification of AKT and high levels of AKT RNA and protein [XREF_BIBR] but also highly active GSK-3beta suggesting that, although some pools of GSK-3 can be phosphorylated by AKT at Ser21 and Ser9 and inhibited, other pools of GSK-3 may remain active in cancer cells [XREF_BIBR]."
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"These mediators activate phosphatidylinositol-3-kinase (PI3K) and Akt which phosphorylates GSK3 at an amino terminal serine residue (Ser21 on GSK3alpha and Ser9 on GSK3beta) creating a pseudo-substrate motif that inhibits the enzyme 's activity and allows activation of downstream effectors like glycogen synthase and the mammalian target of rapamycin (mTOR)."
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"More recently, GSK3 was shown to enhance proteasomal degradation of VEGFR-2 by regulating the binding of β-transducin repeats containing E3 ubiquitin protein ligase to VEGFR-2 (29), and GSK3 activity is inhibited by AKT that phosphorylates the serine residues Ser21 in GSK3α and Ser9 in GSK3β (30)."
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"For instance, two pancreatic cancer cell lines, PANC1 and ASPC1, exhibit amplification of AKT and high levels of AKT RNA and protein [XREF_BIBR] but also highly active GSK-3beta suggesting that, although some pools of GSK-3 can be phosphorylated by AKT at Ser21 and Ser9 and inhibited, other pools of GSK-3 may remain active in cancer cells [XREF_BIBR]."
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"Treatment with 10 µM MK-2206, an Akt inhibitor widely used in the clinical trials for cancer indicated a significant decrease in the expression of phosphorylated Akt, Phosphorylated GSK-3α/β, claudin-5, ZO-1 and ZO-2 protein levels compared to DMSO-treated controls in HLECs (Fig. 5a–d)."
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"Increased phosphorylation of Akt (increased Akt activities) causes phosphorylation of GSK3β (suppression of GSK3β activities) at the serine 9 residue while reduced phosphorylation of Akt (reduced Akt activities) decreases levels of phosphorylation of GSK3β (increased GSK3β activities)."
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"DCT induced PI3K and Akt activation resulted in downstream phosphorylation of GSK-3 (Ser (21/9)) and BAD (Ser (136)), and nuclear translocation (activation) of NF-kappaB, thereby confirming that DCT induced activation of PI3K and Akt signaling regulates both proproliferative and prosurvival signals."
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"DCT induced PI3K and Akt activation resulted in downstream phosphorylation of GSK-3 (Ser (21/9)) and BAD (Ser (136)), and nuclear translocation (activation) of NF-kappaB, thereby confirming that DCT induced activation of PI3K and Akt signaling regulates both proproliferative and prosurvival signals."
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"DCT induced PI3K and Akt activation resulted in downstream phosphorylation of GSK-3 (Ser (21/9)) and BAD (Ser (136)), and nuclear translocation (activation) of NF-kappaB, thereby confirming that DCT induced activation of PI3K and Akt signaling regulates both proproliferative and prosurvival signals."
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"Increased phosphorylation of AKT (increased AKT activities) causes phosphorylation of GSK3β (suppression of GSK3β activities) at the serine 9 residue while reduced phosphorylation of AKT (reduced AKT activities) decreases levels of phosphorylation of GSK3β (increased GSK3β activities) (Beurel et al., 2010)."
"Stable transfection of H1299 NSCLC cells with Akt(DD), another constitutively active form of Akt, stimulated Akt-dependent signalling, as shown by increased expression of P-GSK3 (phosphorylated GSK3) (Figure 1C), and suppressed RA-induced RARB expression (Figure 1D). Together, these findings indicate that activation of Akt inhibits ligand-dependent activation of retinoid receptors."