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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