Gene interactions and pathways from curated databases and text-mining

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GDNF — PIK3R1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Besset et al., J Biol Chem 2000 : In agreement with Ras independent activation of PI3K by GDNF in neuronal cells, survival of sympathetic neurons induced by GDNF was dependent on PI3K but was not affected by microinjection of blocking anti-Ras antibodies, which did compromise neuronal survival by nerve growth factor, suggesting that Ras is not required for GDNF induced survival of sympathetic neurons ... This latter complex can also assemble directly onto phosphorylated Tyr-1096, offering an alternative route to PI3K activation by GDNF
Galaria et al., J Surg Res 2005 : ATF mediated migration is PI3-K dependent and activates two separate pathways : ERK1/2 and akt ... ATF induces akt phosphorylation through a PI3K mediated but ras independent mechanism while both ras and PI3K are required for ERK1/2 activation
Yamaguchi et al., Cancer Res 2006 (Colorectal Neoplasms) : On the other hand, ATF3 expression was not affected by another PI3K inhibitor, wortmannin, as well as phosphatase and tensin homologue or dominant negative Akt overexpression
Shukla et al., Neurotoxicology 2013 : Sal toxicity coincided with reduced pAkt level and its downstream effectors : pCREB, pGSK-3ß, Bcl-2 and neurotrophins GDNF , BDNF suggesting repressed PI3K/Akt signaling