◀ Back to STAT3
KIT — STAT3
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
STAT3
→
KIT
(increases, KIT Activity)
Evidence: STAT3 is activated by many interleukins, IFNg,c-Kit, SCF, GCSF and EGF (for a review, see Heinrich et al., 2003) similar to STAT5, which is activated in particular by IL-2 and IL-7, Prolactin, G-CSF and GM-CSF.
-
KEGG Acute myeloid leukemia:
KIT
→
STAT3/STAT5A/STAT5B
(protein-protein, activation)
-
Reactome Reaction:
KIT
→
STAT3
(indirect_complex)
Brizzi et al., J Biol Chem 1999, Ning et al., Oncogene 2001, Deberry et al., Biochem J 1997
-
Reactome Reaction:
KIT
→
STAT3
(reaction)
Brizzi et al., J Biol Chem 1999, Ning et al., Oncogene 2001, Deberry et al., Biochem J 1997
Text-mined interactions from Literome
Duensing et al., Oncogene 2004
(Gastrointestinal Neoplasms) :
Using GIST in vitro models, we showed that activation of MAPK p42/44, AKT, and S6K was KIT dependent, whereas STAT1 and
STAT3 phosphorylation was only partially
dependent on
KIT activation
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