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TGFB3 — TIMP3

Text-mined interactions from Literome

Qureshi et al., Biochim Biophys Acta 2008 : Smad signaling pathway is a pivotal component of tissue inhibitor of metalloproteinases-3 regulation by transforming growth factor beta in human chondrocytes
Morris et al., Connect Tissue Res 2010 : Stimulation with Interleukin-1ß and osteogenic protein-1 decreased while tumor necrosis factor alpha and transforming growth factor beta increased TIMP-3 protein levels ; however, TIMP-3 mRNA was not significantly affected by any of these treatments
Su et al., DNA Cell Biol 1996 (Osteoarthritis) : Regulation of tissue inhibitor of metalloproteinases-3 gene expression by transforming growth factor-beta and dexamethasone in bovine and human articular chondrocytes
Mattila et al., J Invest Dermatol 1998 (Scleroderma, Localized) : Specific activation of TIMP-3 gene expression in scleroderma skin fibroblasts in culture and in vivo suggests a role for TIMP-3 in the pathogenesis of dermal fibrosis via inhibition of turnover of fibrotic dermal extracellular matrix, possibly due to upregulation of TIMP-3 expression by transforming growth factor-beta
Huang et al., J Clin Endocrinol Metab 1998 : We have investigated the roles of IL-1 beta and transforming growth factor-beta ( TGF beta ) in regulating TIMP-1, TIMP-3 , and 92-kDa type IV collagenase messenger ribonucleic acid ( mRNA ) expression in human endometrial stromal cells using quantitative competitive PCR
Fabunmi et al., Circ Res 1998 (Arteriosclerosis) : Human smooth muscle cells constitutively expressed TIMP-1, -2 and -3 proteins ; platelet derived growth factor and transforming growth factor-beta augmented levels of TIMP-1 and TIMP-3 but not TIMP-2