Gene interactions and pathways from curated databases and text-mining

◀ Back to TGFB1

TGFB1 — TIMP3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Hoshino et al., Respiration 2001 : Interleukin-1beta (IL-1beta) and transforming growth factor-beta1 ( TGF-beta1 ) increased MMP-3 and TIMP-3 expressions in A549 cells in a time- and concentration dependent manner ... IL-1beta mainly augmented MMP-3 expression, while TGF-beta1 mainly augmented TIMP-3 expression
Salmela et al., Mod Pathol 2003 (Graft vs Host Disease) : In agreement with previous data on cancer cells, TIMP-3 , induced by TGF-beta1 , may contribute to the apoptosis of keratinocytes in cutaneous graft-versus-host disease lesions, leading to typical histopathological changes
Li et al., Free Radic Biol Med 2004 : Transforming growth factor Beta1 induction of tissue inhibitor of metalloproteinases 3 in articular chondrocytes is mediated by reactive oxygen species ... TGF-beta1 induces tissue inhibitor of metalloproteinases 3 ( TIMP-3 ), an inhibitor of cartilage damaging matrix metalloproteianases and aggrecanases ... We investigated the role of reactive oxygen species ( ROS ) in TIMP-3 induction by TGF-beta1 ... The TIMP-3 increase induced by TGF-beta1 was partly Smad2 dependent ... Reduced glutathione and L-cysteine also blocked Smad2 and TIMP-3 induction by TGF-beta1 , whereas a nonthiol, N-acetylalanine, did not
Cross et al., Prostate 2005 (Prostatic Hyperplasia...) : In stromal cells, TGFbeta1 decreased ADAMTS-1, -5, -9, and -15 transcripts and increased ADAMTS-4, versican, and TIMP-3
García-Alvarez et al., Exp Lung Res 2006 (Pulmonary Fibrosis) : The authors examined whether the MAPK pathway was involved in TGF-beta1 induced TIMP3 expression ... Our findings suggest that TGF-beta1 induced TIMP3 may be an important mediator in lung fibrogenesis
Qureshi et al., Cell Signal 2007 : This study tested the hypothesis that Akt/protein kinase B signaling pathway could mediate TGF-beta1 induction of TIMP-3 in human articular chondrocytes
Tsuji et al., Spine (Phila Pa 1976) 2007 : Decrease in expression of TIMP-3 , possibly mediated in part by TGF-beta1 , may cause imbalance of ADAMTS4/TIMP-3 ratio at transition period from notochordal to fibrocartilaginous NP
El Mabrouk et al., J Cell Biochem 2008 : IL-4 also downregulated TGF-beta1 induced TIMP-3 gene expression, Smad2, and JNK phosphorylation
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 ... Here we investigated previously unexplored roles of specific Smads in TGF-beta1 induction of TIMP-3 gene by pharmacological and genetic knockdown approaches ... TGF-beta1 induced Smad2 phosphorylation and TIMP-3 protein expression could be inhibited by the Smad2/3 phosphorylation inhibitors, PD169316 and SB203580 and by Smad2-specific siRNA
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
Leco et al., J Biol Chem 1994 : Like TIMP-1, TIMP-3 was highly inducible in mouse C3H 10T1/2 fibroblasts by phorbol ester ( PMA ), epidermal growth factor (EGF), and transforming growth factor-beta 1 , but nuclear run-on assays showed that the on/off transcription kinetics were faster for TIMP-3 than TIMP-1
Gatsios et al., Eur J Biochem 1996 : We found that transforming growth factor beta 1 as well as interleukin-1 beta induce gene expression of both TIMP-1 and TIMP-3
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