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TGFB1 — THBS3

Text-mined interactions from Literome

Janat et al., J Cell Physiol 1992 : We have studied the effect of transforming growth factor beta 1 ( TGF-beta 1 ) on vascular smooth muscle cell ( SMC ) mitogenesis and expression of thrombospondin and other growth related genes ... Although TGF-beta 1 was able to directly enhance expression of thrombospondin as well as the growth related genes c-fos and c-myc, and induced c-fos expression with identical kinetics as PDGF, it was unable to elicit [ 3H ] thymidine incorporation into DNA in three independent smooth muscle cell strains ... Our results strongly suggest that induction of thrombospondin expression by TGF-beta 1 and by PDGF occurs by distinct mechanisms ... In addition, that TGF-beta 1 can enhance PDGF induced mitogenesis may be due to the ability of TGF-beta 1 to directly induce the expression of thrombospondin , c-fos, c-myc, and the PDGF beta-receptor
Horiguchi et al., Endocrine 2004 : Regulation of VEGF-A, VEGFR-I, thrombospondin-1 , -2, and -3 expression in a human pituitary cell line ( HP75 ) by TGFbeta1 , bFGF, and EGF
Hsu et al., Cancer Res 1996 (Brain Neoplasms...) : This change in angiogenesis was directly due to the increased secretion of a potent inhibitor of angiogenesis, thrombospondin-1, because : ( a ) neutralizing thrombospondin completely relieved the inhibition ; ( b ) the inhibitory activity of thrombospondin was not dependent on transforming growth factor beta ; and ( c ) chromosome 10 introduction did not alter secreted inducing activity
Jakowlew et al., Biochim Biophys Acta 1997 (Carcinoma, Non-Small-Cell Lung...) : To investigate the relationship between plasminogen activator (PA), plasminogen activator inhibitor-1 ( PAI-1 ) and the extracellular matrix in malignant and normal lung epithelial cells and to determine whether malignant lung epithelial cells may be more invasive than normal lung epithelial cells because of differences in expression of these proteins in response to TGF-beta, the regulation of PA, PAI-1, fibronectin, laminin and thrombospondin by TGF-beta1 in human non-small cell lung cancer ( NSCLC ) cells was examined and compared with normal human bronchial epithelial ( NHBE ) cells
Basile et al., Curr Opin Nephrol Hypertens 1999 (Kidney Diseases) : Both in-vitro and in-vivo studies have demonstrated that proteolytic activity, thrombospondin-1 , elevated glucose, angiotensin II, oxidant stress and hemodynamic forces regulate transforming growth factor beta activity through both transcriptional and post-transcriptional mechanisms