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CDKN1A — PI3

Text-mined interactions from Literome

Hmama et al., J Exp Med 1999 : These findings suggest that PI 3-kinase selectively regulates D ( 3 ) -induced monocyte differentiation, independent of any effects on p21
Mitsuuchi et al., Cancer Res 2000 (Ovarian Neoplasms) : Here, we demonstrate that phosphatidylinositol 3-kinase (PI3K) and its downstream targets serine/threonine kinases AKT1 and AKT2 ( AKT ), are required for the full induction of p21 in A2780 cells treated with cisplatin or paclitaxel
Lawlor et al., J Cell Biol 2000 : Unexpectedly, loss of MyoD expression did not impede IGF mediated survival, revealing a second pathway involving activation by PI3-kinase of Akt, and subsequent induction of p21
Hiromura et al., Kidney Int 2002 : Our results also showed that the CDK-inhibitor p21 was increased by insulin and that p21 up-regulation was PI3-kinase/Akt pathway dependent
Oh et al., Exp Mol Med 2002 (Colorectal Neoplasms...) : In this study, we have elucidated differential regulation of the zinc stimulated p21 ( CiP/WAF1 ) and cyclin D1 activation by inhibition of phosphoinositide 3-kinase (PI3K)
Linnemann et al., Virology 2002 : Moreover, PI3K was required to activate the Nef associated p21 activated kinase (PAK)
Comalada et al., Eur J Immunol 2004 : PI-3K inhibitors also block growth factor dependent expression of p21 ( Waf1 ) and the activation of Akt
Bond et al., Cardiovasc Res 2006 : Interestingly, levels of endogenous p21Cip1 and Skp2 were both increased in a phosphoinositide PI 3-kinase dependent manner in late G1 phase
Santra et al., J Cereb Blood Flow Metab 2006 (Glioma) : Blocking of phosphoinositide 3-kinase (PI-3K) , Ras, and the epidermal growth factor receptor with specific inhibitors had no effect on induction of Ras, p21 , and p27 at the messenger RNA level in decorin synthesizing SVZ and U-87 cells
Wang et al., PloS one 2007 : Furthermore, we show here a novel mechanism for NRP-1-specific control of the anti-apoptotic pathway in EC through involvement of the NRP-1 interacting protein ( NIP/GIPC ) in the activation of PI-3K/Akt and subsequent inactivation of p53 pathways and FoxOs, as well as activation of p21
Yohn et al., BMC urology 2011 (Carcinoma, Transitional Cell...) : PI3-kinase and AKT cause an upregulation of p21 by suppressing GSK-3ß activity and activating mTOR in both cultured human urothelial carcinoma cells and mouse urothelial cells in vivo