The activation of Akt/PKB signaling pathway and cell survival

By G. Song, G. Ouyang, S. Bao. Journal of Cellular and Molecular Medicine, 2005

1,986 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Akt Signaling Pathway in Macrophage Activation and M1/M2 Polarization (2017, background): “Activated PI3K type I phosphorylates phosphatidylinositol 4,5-bisphosphate (PIP2) to generate phosphatidylinositol 3,4,5-triphosphate (PIP3) at the plasma membrane; PIP3 further recruits Akt and the mechanistic target of rapamycin complex (mTORC) 2, and facilitates Akt activation by mTORC2 (13, 14).”
Fuel feeds function: energy metabolism and the T-cell response (2005, neutral): “For in-depth discussion, see several recent review”
Human T-cell leukaemia virus type 1 (HTLV-1) infectivity and cellular transformation (2007, background): “Akt is regulated by phosphatidylinositol 3-kinase ( PI3K ) through site-specific phosphorylation, primarily on Ser473 (Ref”
CD28− T cells: their role in the age-associated decline of immune function (2009, background): “It has been shown that the kinase Akt (protein kinase B, PKB) signaling is crucial for cell proliferation, survival [73], and telomerase induction [74].”
Amiloride inhibits macropinocytosis by lowering submembranous pH and preventing Rac1 and Cdc42 signaling (2010, background): “Akt becomes phosphorylated at the membrane by PDK1 and 2, which are themselves PIP3-activated kinases (Cantley, 2002; Song et al., 2005).”