◀ Back to STAT1
IL2 — STAT1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database IL2-mediated signaling events:
STAT1 (STAT1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3)
(modification, collaborate)
Delespine-Carmagnat et al., Eur J Immunol 2000, Frank et al., Proc Natl Acad Sci U S A 1995, Hou et al., Immunity 1995
Evidence: assay, physical interaction
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3)
→
STAT1 (dimer) complex (STAT1)
(modification, activates)
Delespine-Carmagnat et al., Eur J Immunol 2000, Frank et al., Proc Natl Acad Sci U S A 1995, Hou et al., Immunity 1995
Evidence: assay, physical interaction
-
NCI Pathway Database IL12-mediated signaling events:
STAT1 (STAT1)
→
IL2/IL2R complex (IL2RA-IL2RB-IL2RG-IL2)
(modification, collaborate)
Gollob et al., J Immunol 1999
Evidence: mutant phenotype, assay
Text-mined interactions from Literome
Gollob et al., J Immunol 1999
:
A specific inhibitor of p38 MAP kinase completely inhibits the serine phosphorylation of
STAT1 and STAT3
induced by IL-12 and
IL-2 and abrogates the functional synergy between IL-12 and IL-2 without affecting STAT tyrosine phosphorylation
Subramaniam et al., Biochem Biophys Res Commun 1999
:
Immunoprecipitation with specific antibodies followed by Western blot analysis with antiphosphotyrosine antibody has shown that in U937 cells,
interleukin-17 induces time dependent stimulation of tyrosine phosphorylation of JAK 1, 2 and 3, Tyk 2 and
STAT 1 , 2, 3 and 4 within 0.5 to 30 min. Interleukin-17 mediated tyrosine phosphorylation of these proteins strongly suggests that the JAK/STAT signaling pathway may play a major role in transducing signals from interleukin-17 receptors to the nucleus
Lee et al., J Exp Med 1999
:
Interestingly,
interleukin (IL)-7 selectively
activated STAT1 and induced MHC class I in mature T but not B cells
Owaki et al., J Immunol 2006
:
Analyses using various mice lacking a signaling molecule revealed that the inhibition of
IL-2 production was
dependent on
STAT1 , but not on STAT3, STAT4, and T-bet, and was highly correlated with the induction of SOCS3 expression
Tomic et al., J Immunol 2006
(Leukemia, Lymphocytic, Chronic, B-Cell...) :
IL-2 with S28690 caused CLL cells to proliferate and
increased their expression of B7-family members, production of TNF-alpha and IL-10, and levels of tyrosine phosphorylated
STAT-1 and STAT-3 proteins
Beadling et al., EMBO J 1994
:
IFN alpha activated
STAT1 , STAT2 and STAT3 in T cells, but no detectable activation of these STATs was
induced by
IL-2
Yu et al., J Immunol 1996
:
IL-2 induced less
STAT1 alpha activation and IFN-alpha induced greater STAT5 activation in NK3.3 cells compared with preactivated primary NK cells
Wang et al., J Immunol 1999
:
In both T cells and NK cells,
IL-2 induces the activation of
STAT1 , STAT3, and STAT5