@article {GUO1337, author = {BAOQIANG GUO and MARK SLEVIN and CHENGGANG LI and SUDEEP PARAMESHWAR and DONGHUI LIU and PAT KUMAR and CARMELO BERNABEU and SHANT KUMAR}, title = {CD105 Inhibits Transforming Growth Factor-{\ss}-Smad3 Signalling}, volume = {24}, number = {3A}, pages = {1337--1346}, year = {2004}, publisher = {International Institute of Anticancer Research}, abstract = {CD105 (endoglin) is an important component of the transforming growth factor-β (TGF-β) receptor complex and is highly expressed in endothelial cells in tissues undergoing angiogenesis such as healing wounds, infarcts and in a wide range of tumours. In an attempt to understand the molecular mechanism by which CD105 exerts its effects on angiogenesis by modulating TGF- β1 signalling, in this preliminary communication, CD105 transfected rat myoblasts were utilized as an in vitro model. Overexpression of CD105 in these transfectants antagonised TGF-β1-mediated inhibition of cell proliferation and reduced TGF-β1-mediated p3TP-Lux (PAI-1 promoter) luciferase activity. It also reduced (CAGA)12-Luc luciferase activity in response to TGF-β1. The CAGA sequence is specific for Smad3/4 binding, implying that CD105 is involved in inhibition of TGF- β1/Smad3 signalling. Furthermore, CD105 overexpression reduced serine phosphorylation of Smad3 and inhibited subsequent nuclear translocation of Smad3. CD105 resulted in high phosphorylation of JNK1, which is able to activate c-Jun. c-Jun is known to inhibit Smad3 transcriptional activity on CAGA sites, suggesting that CD105 may also inhibit Smad3 signalling through JNK1. Copyright{\textcopyright} 2004 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/24/3A/1337}, eprint = {https://ar.iiarjournals.org/content/24/3A/1337.full.pdf}, journal = {Anticancer Research} }