◀ Back to PIK3CA
KIT — PIK3CA
Pathways - manually collected, often from reviews:
-
KEGG Pathways in cancer:
KIT
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Acute myeloid leukemia:
KIT
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
Reactome Reaction:
KIT
→
PIK3CA
(reaction)
Chian et al., Blood 2001*, Rönnstrand et al., Cell Mol Life Sci 2004*, Reber et al., Eur J Pharmacol 2006, Sun et al., J Biol Chem 2008
-
Reactome Reaction:
KIT
→
PIK3CA
(indirect_complex)
Chian et al., Blood 2001*, Rönnstrand et al., Cell Mol Life Sci 2004*, Reber et al., Eur J Pharmacol 2006, Sun et al., J Biol Chem 2008
Text-mined interactions from Literome
Ueda et al., Blood 2002
(Calcium Signaling) :
In Y719F, the binding of phosphatidylinositol 3'-kinase (PI3K) to
KIT was lost and KIT mediated cell migration and Ca ( 2+ ) mobilization were
suppressed by PI3K chemical inhibitors or dominant negative
PI3K , suggesting the involvement of Y719 mediated PI3K pathway in cell migration
Koma et al., Lab Invest 2005
:
KIT-Y719F does not
activate PI3-K , whereas KIT-Y821F does
Zhu et al., Oncogene 2007
(Gastrointestinal Stromal Tumors) :
Activated signaling intermediates were identified by immunoaffinity purification of tyrosine phosphorylated proteins in GIST cells before and after treatment with KIT inhibitors, and these analyses show that GRB2, SHC, CBL and MAPK activation are largely KIT dependent in GISTs, whereas
PI3-K , STAT1 and STAT3 activation are partially
KIT dependent