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COL1A2 — SP1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Poncelet et al., J Biol Chem 2001
:
Chemical inhibition of
Sp1 binding with mithramycin A, or deletion of the GC boxes,
inhibited COL1A2 activation by Smad3, suggesting cooperation between Smad3 and Sp1 in the TGF-beta1 response ... Finally, combined
Sp1 and Smad3 overexpression
induces marked ligand independent and ligand dependent promoter activity of
COL1A2
Inagaki et al., J Biol Chem 2001
:
Transfection of HSC with an Sp3 expression plasmid abolished the COL1A2 response to TGF-beta, whereas overexpression of
Sp1 in hepatocytes
increased basal
COL1A2 transcription and conferred TGF-beta responsiveness
Ihn et al., Rheumatology (Oxford) 2006
(Scleroderma, Systemic) :
The overexpression of
Sp1 caused further increase in
COL1A2 promoter activity stimulated by TGF-beta in normal fibroblasts, but did not change COL1A2 promoter activity in the presence of TGF-beta in SSc fibroblasts
Yang et al., Biochem Biophys Res Commun 2008
(Liver Cirrhosis) :
We found that PL decreases the promoter activity of
Col 1A2 , hinders the translocalization of phosphorylated Smad2/3-Smad 4 complex from cytosol into nucleus and
inhibits Sp1 binding activity