IndraLab
Statements
eidos
"Specifically , PTEN dephosphorylates PIP3 , preventing Akt1 activation , thereby directly antagonizing the PI3K function and blocking , therefore the activation of downstream signaling events , including PDK1 , ( Akt ) and Akt / mammalian target of rapamycin ( mTOR ) ( Gingras et al ., 2001 ) ."
reach
"Akt1/2 deletion results in inhibited proliferation of HSCs and impaired long-term function (Juntilla et al., 2010), while aberrant activation of Akt-mTOR signaling by PTEN deletion or overexpression of Akt1 leads to quiescence exit and eventual exhaustion of HSCs (Yilmaz et al., 2006; Kharas et al., 2010)."
reach
"Recent studies have shown that a loss of PTEN causes continuous activation of protein kinase B (Akt), which is critical in the phosphoinositide 3-kinase (PI3K)-Akt pathway that leads to cell proliferation.9, 10, 11 When NSCLC with low PTEN expression is treated with TKIs, resistance will occur.12 Therefore, TKI resistance could be reversed by upregulating PTEN expression levels."