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IL3 — SOAT1
Text-mined interactions from Literome
Matsumura et al., EMBO J 1999
:
In electrophoretic mobility shift assays,
STAT5 bound to the element in
response to
IL-3
Le et al., J Biol Chem 2000
(MAP Kinase Signaling System) :
Moreover, the mutations abolished
IL-3 induced JAK2,
STAT , and AKT activation in the unselected cells, whereas activation of these molecules in IL-3 selected cells was normal
Gesbert et al., Blood 2000
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
Interestingly, however,
STAT5-1*6 required the continued presence of
IL-3 to cause a significant increase in Bcl-X ( L ) protein, whereas p210 ( Bcr/Abl ) did not need IL-3
Wheadon et al., Blood 2003
:
We demonstrate that TEL/PDGFbetaR expression augmented
IL-3 induced
activation of PKB,
STAT5 , ERK1/2, p38, and JNK1/2
Yu et al., Oncogene 2003
:
Further biochemical analyses revealed that
IL-3 induced
Jak/Stat , Erk, and PI3 kinase pathways in SHP-2 ( -/- ) cells were impaired and reintroduction of WT SHP-2 into mutant cells partially restored IL-3 signaling
Natarajan et al., Glia 2004
(Encephalitis...) :
In this study, we found that in vitro treatment of EOC-20 microglial cells with tyrphostin AG490 blocked
IL-3 induced tyrosine phosphorylation of JAK2,
STAT5A , and STAT5B signaling proteins
Tannahill et al., Mol Cell Biol 2005
:
Unlike other SOCS family members, we find that SOCS2 can enhance interleukin-2 (IL-2)- and
IL-3 induced
STAT phosphorylation following and potentiate proliferation in response to cytokine stimulation
Pecaric-Petkovic et al., Blood 2009
(Hypersensitivity) :
These effects are similar to that of IL-3, but the signaling pathways engaged are distinct because IL-33 strongly activates NF-kappaB and shows a preference for p38 MAP-kinase, while
IL-3 acts through
Jak/Stat and preferentially activates ERK
Seidel et al., Proc Natl Acad Sci U S A 1995
(Carcinoma, Hepatocellular...) :
We have systematically examined the effects of the spacing between the TT and AA core half sites on the binding of the
STAT complexes
activated by IFN-gamma,
interleukin (IL) 6, granulocyte-macrophage colony stimulating factor, and IL-4