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SERPINB2 — TNF

Text-mined interactions from Literome

Mahony et al., Eur J Biochem 1999 (Fibrosarcoma) : Here we have examined whether PAI-2 gene transcription in response to TNFalpha may be mediated through a regulatory pathway involving the transcription factor, NF-kappaB ... While no evidence was found for TNFalpha regulation of the PAI-2 gene through either of these two sites, one of the NF-kappaB-like motifs, transcriptional regulatory motif ( TRM ), present at position -400 was found to be essential for constitutive PAI-2 transcription, as mutation of this motif abolished basal PAI-2 promoter activity in both monocyte-like U937 cells and HT1080 fibrosarcoma cells
Idell et al., Am J Respir Cell Mol Biol 1992 (Inflammation...) : PAI-2 release is induced by TNF-alpha and TGF-beta
Muth et al., Crit Care Med 2004 : In all EC, stimulation with tumor necrosis factor-alpha and lipopolysaccharide increased the expression of PAI-1, PAI-2 , and u-PA and decreased t-PA expression
Fish et al., Exp Cell Res 2006 (Colonic Neoplasms...) : In conclusion, elevated PAI-2 levels do not protect cells from TNF-alpha induced apoptosis, and the protective effect of prior stimulation with TNF-alpha does not require PAI-2
Johnson et al., J Biol Chem 1990 (Melanoma) : In addition, induction of PAI-2 synthesis by TNF was blocked by two PKC inhibitors, staurosporine and 1- ( 5-isoquinolinesulfonyl ) -2-methylpiperazine dihydrochloride ... In contrast to the positive regulation by PKC in promoting TNF induced PAI-2 synthesis cAMP inhibited this response ... Pretreatment of cells with agents that raise intracellular cAMP levels completely abolished TNF induced PAI-2 synthesis ... PAI-2 mRNA accumulation in response to TNF was inhibited, but not completely abolished, by cAMP elevating agents, suggesting that cAMP also exerted its inhibitory effect at the translation level
Scarpati et al., J Biol Chem 1989 : By 3-5 h, PMA or TNF induced both tissue factor and PAI-2 to approximately 150-420 mRNA molecules/cell and both mRNAs declined to basal levels within several hours ; however, PAI-1 and thrombomodulin mRNA levels did not change
Zoellner et al., Thromb Haemost 1993 : IL-1 alpha and TNF alpha increased the synthesis of PAI-2 and PAI-1 by EC in a dose dependent manner
Maurer et al., J Biol Chem 1996 (Fibrosarcoma) : TNF and PMA co-treatment of transfected cells increases beta-globin-PAI-2 chimeric mRNA expression 3-4-fold, indicating that the inherently unstable 3'-UTR of PAI-2 mRNA can become stabilized in response to TNF and PMA ... Our results indicate that induction of PAI-2 gene expression by TNF and PMA involves both direct transcription as well as mRNA stabilization, the latter involving an AU-rich nonameric motif in the 3'-UTR
Dear et al., Eur J Biochem 1996 : Removal of the proximal repressor by deletion to position -219, or by internal deletion from the -1100 PAI-2 CAT construct, resulted in a selective increase in TNF responsiveness, suggesting that induction of PAI-2 gene transcription by TNF is associated with derepression ... However, treatment of cells with TNF results in a profound selective reduction in site-B binding activity, suggesting that this site plays a significant role in TNF mediated regulation of PAI-2 gene expression ... Our findings suggest that TNF mediated induction of PAI-2 gene expression involves derepression and is associated with cis acting and trans acting factors located within and adjacent to the proximal repressor region
Antalis et al., J Exp Med 1998 : These observations, together with the recently demonstrated PAI-2 mediated inhibition of tumor necrosis factor-alpha induced apoptosis, ( a ) illustrate that PAI-2 has an additional and distinct function as an intracellular regulator of signal transduction pathway ( s ) and ( b ) demonstrate a novel activity for a eukaryotic serpin