TY - JOUR
T1 - A self-enabling TGFβ response coupled to stress signaling
T2 - Smad engages stress response factor ATF3 for Id1 repression in epithelial cells
AU - Kang, Yibin
AU - Chen, Chang Rung
AU - Massagué, Joan
PY - 2003/4/1
Y1 - 2003/4/1
N2 - Genome-wide transcriptional profiling of human epithelial cells revealed that repression of Id inhibitors of differentiation (Id1, Id2, and Id3) is a general feature of the TGFβ cytostatic program. Opposite responses of Id1 to TGFβ and the related factor BMP are dictated by the specific ability of the TGFβ mediator, Smad3, to activate expression of stress response factor ATF3 and then recruit this factor to the Id1 promoter. Thus, a Smad3-mediated primary gene response, ATF3 induction, enables Smad3 to participate in an ATF3-mediated, secondary gene response. As a common target of TGFβ/Smad signals and stress signals via p38 kinase, ATF3 additionally serves to channel synergy between these pathways in the response of epithelial cells to stress and injury.
AB - Genome-wide transcriptional profiling of human epithelial cells revealed that repression of Id inhibitors of differentiation (Id1, Id2, and Id3) is a general feature of the TGFβ cytostatic program. Opposite responses of Id1 to TGFβ and the related factor BMP are dictated by the specific ability of the TGFβ mediator, Smad3, to activate expression of stress response factor ATF3 and then recruit this factor to the Id1 promoter. Thus, a Smad3-mediated primary gene response, ATF3 induction, enables Smad3 to participate in an ATF3-mediated, secondary gene response. As a common target of TGFβ/Smad signals and stress signals via p38 kinase, ATF3 additionally serves to channel synergy between these pathways in the response of epithelial cells to stress and injury.
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U2 - 10.1016/S1097-2765(03)00109-6
DO - 10.1016/S1097-2765(03)00109-6
M3 - Article
C2 - 12718878
AN - SCOPUS:0038369998
SN - 1097-2765
VL - 11
SP - 915
EP - 926
JO - Molecular Cell
JF - Molecular Cell
IS - 4
ER -