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IL2 — SMAD3
Text-mined interactions from Literome
Tzachanis et al., Nat Immunol 2001
:
The inhibitory effect of Tob on
interleukin 2 (IL-2) transcription was not
mediated by blockade of NFAT, AP-1 or NF-kappaB transactivation but by enhancement of
Smad binding on the -105 negative regulatory element of the IL-2 promoter
Verrecchia et al., J Biol Chem 2003
:
We demonstrate that, in a cellular context devoid of JNK activity ( i.e. jnk ( -/- ) fibroblasts ),
interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) did not
inhibit the formation of SMAD-DNA complexes and the resulting
SMAD-driven transcription in response to TGF-beta
Wakabayashi et al., J Biol Chem 2011
:
Here, we demonstrate that Smad2 and
Smad3 , two major TGF-ß-downstream transcription factors, are redundantly
essential for TGF-ß mediated suppression of
IL-2 production in CD4 ( + ) T cells using Smad2- and Smad3-deficient T cells
Yoshioka et al., Eur J Immunol 2012
:
Dorsomorphin efficiently suppressed IL-2 production even at low doses in mouse CD4 ( + ) T cells, suggesting that the
BMP-Smad signalling physiologically
regulates IL-2 transcription in these cells
Battaglia et al., Immunology 2013
:
Treg cell reduction was related to persistent activation of Stat3, a negative regulator of Treg cells associated with down-modulation of
IL-2/TGF-ß induced phosphorylation of
Smad2/3 , a positive regulator of Treg cells
Meisel et al., Immunity 2013
(Encephalomyelitis, Autoimmune, Experimental) :
Furthermore, PKCa-deficient ( Prkca ( -/- ) ) cells demonstrated a defect in
SMAD dependent
IL-2 suppression, as well as decreased STAT3 DNA binding within the Il17a promoter