◀ Back to PIK3R1
GDNF — PIK3R1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET9/GFRalpha1/GDNF/SHC/GAB1/Grb2 complex (RET-GFRA1-GDNF-SHC1-GRB2-GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Hennige et al., Mol Cell Endocrinol 2000, Hayashi et al., Oncogene 2000, Maeda et al., Biochem Biophys Res Commun 2004
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF/SHC/GAB1/Grb2 complex (RET-GFRA1-GDNF-SHC1-GRB2-GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Hennige et al., Mol Cell Endocrinol 2000, Hayashi et al., Oncogene 2000, Maeda et al., Biochem Biophys Res Commun 2004
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET9/GFRalpha1/GDNF/Shank3/Grb2 complex (RET-SHANK3-GRB2-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Schuetz et al., J Cell Biol 2004
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF complex (RET-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Fukuda et al., J Biol Chem 2002
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF/IRS1 complex (RET-IRS1-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Melillo et al., Oncogene 2001
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF complex (RET-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Murakami et al., Oncogene 1999
Evidence: assay, physical interaction
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