Smad7 differentially regulates transforming growth factor beta-mediated signaling pathways. Export

@article{citeulike:2521670, abstract = {Smad7 has been identified as a negative regulator of transforming growth factor beta (TGF-beta) signaling by interfering with the phosphorylation of other Smad proteins by TGF-beta receptor type I (TbetaRI). We established a mink lung epithelial (Mv1Lu) cell line where ectopic expression of Smad7 is tightly controlled by doxycycline using an improved Tet-on system. Once induced by doxycycline, the recombinant Smad7 was localized predominantly in the perinuclear region and in the cytoplasm. However, the type of culture surface alters the subcellular localization of Smad7: on plastic or on fibronectin-coated glass, Smad7 was localized in the cytoplasm; but when the cells were cultured on glass, nuclear localization was observed. TGF-beta stimulation did not alter substantially the cellular distribution of Smad7. Importantly, the expression of recombinant Smad7 differentially inhibited TGF-beta signaling pathways. Consistent with previous studies, Smad7 inhibited TGF-beta-stimulated induction of type 1 plasminogen activator inhibitor as measured by p3TP-Lux reporter. However, expression of Smad7 had little effect on TGF-beta-induced growth inhibition.}, address = {Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria 3050, Australia. Hong.Jian.Zhu@ludwig.edu.au}, author = {Zhu, H. J. and Iaria, J. and Sizeland, A. M.}, citeulike-article-id = {2521670}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/10542264}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=10542264}, day = {5}, issn = {0021-9258}, journal = {J Biol Chem}, keywords = {signalisation, smads}, month = {November}, number = {45}, pages = {32258--32264}, posted-at = {2008-03-12 16:17:54}, priority = {2}, title = {Smad7 differentially regulates transforming growth factor beta-mediated signaling pathways.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/10542264}, volume = {274}, year = {1999} }

TY - JOUR ID - citeulike:2521670 L3 - citeulike-article-id:2521670 N2 - Smad7 has been identified as a negative regulator of transforming growth factor beta (TGF-beta) signaling by interfering with the phosphorylation of other Smad proteins by TGF-beta receptor type I (TbetaRI). We established a mink lung epithelial (Mv1Lu) cell line where ectopic expression of Smad7 is tightly controlled by doxycycline using an improved Tet-on system. Once induced by doxycycline, the recombinant Smad7 was localized predominantly in the perinuclear region and in the cytoplasm. However, the type of culture surface alters the subcellular localization of Smad7: on plastic or on fibronectin-coated glass, Smad7 was localized in the cytoplasm; but when the cells were cultured on glass, nuclear localization was observed. TGF-beta stimulation did not alter substantially the cellular distribution of Smad7. Importantly, the expression of recombinant Smad7 differentially inhibited TGF-beta signaling pathways. Consistent with previous studies, Smad7 inhibited TGF-beta-stimulated induction of type 1 plasminogen activator inhibitor as measured by p3TP-Lux reporter. However, expression of Smad7 had little effect on TGF-beta-induced growth inhibition. IS - 45 JF - J Biol Chem SN - 0021-9258 AD - Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria 3050, Australia. Hong.Jian.Zhu@ludwig.edu.au EP - 32264 TI - Smad7 differentially regulates transforming growth factor beta-mediated signaling pathways. VL - 274 SP - 32258 KW - signalisation KW - smads AU - Zhu, HJ AU - Iaria, J AU - Sizeland, AM PY - 1999/11/05/ UR - http://view.ncbi.nlm.nih.gov/pubmed/10542264 ER -