HTLV-1 bZIP factor enhances TGF-β signaling through p300 coactivator
T Zhao, Y Satou, K Sugata, P Miyazato… - Blood, The Journal …, 2011 - ashpublications.org
T Zhao, Y Satou, K Sugata, P Miyazato, PL Green, T Imamura, M Matsuoka
Blood, The Journal of the American Society of Hematology, 2011•ashpublications.orgCtgf, Foxp3, Runx1, and Tsc22d1 genes and suppression of the Id2 gene; such effects were
similar to those by TGF-ß. In particular, HBZ induced Foxp3 expression in naive T cells
through Smad3-dependent TGF-ß signaling. Our results suggest that HBZ, by enhancing
TGF-ß signaling and Foxp3 expression, enables HTLV-1 to convert infected T cells into
regulatory T cells, which is thought to be a critical strategy for virus persistence.(Blood. 2011;
118 (7): 1865-1876)
similar to those by TGF-ß. In particular, HBZ induced Foxp3 expression in naive T cells
through Smad3-dependent TGF-ß signaling. Our results suggest that HBZ, by enhancing
TGF-ß signaling and Foxp3 expression, enables HTLV-1 to convert infected T cells into
regulatory T cells, which is thought to be a critical strategy for virus persistence.(Blood. 2011;
118 (7): 1865-1876)
Ctgf, Foxp3, Runx1, and Tsc22d1 genes and suppression of the Id2 gene; such effects were similar to those by TGF-ß. In particular, HBZ induced Foxp3 expression in naive T cells through Smad3-dependent TGF-ß signaling. Our results suggest that HBZ, by enhancing TGF-ß signaling and Foxp3 expression, enables HTLV-1 to convert infected T cells into regulatory T cells, which is thought to be a critical strategy for virus persistence.(Blood. 2011; 118 (7): 1865-1876)
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