Gene interactions and pathways from curated databases and text-mining

◀ Back to IRF6

IRF6 — SERPINB2

Text-mined interactions from Literome

Ritchie et al., Exp Cell Res 2000 : This study shows that thrombin or LPS protected monocytes from apoptosis and that PAI-2 did not mediate this inhibitory effect
Xiao et al., J Periodontal Res 2001 : The aim of the present study was to investigate the effect of lipopolysaccharide (LPS) on the synthesis of t-PA and PAI-2 by human gingival fibroblasts (HGF) ... The results showed t-PA synthesis was increased in response to all types of LPS studied and PAI-2 level was increased by LPS from A. actinomycetemcomitans and F. nucleatum, but not P. gingivalis
Hamilton et al., Blood 1992 : Lipopolysaccharide (LPS) increased both extracellular and cell associated PAI-2 levels, as well as PAI-2 mRNA measured by Northern analysis
Rossiello et al., Toxicol Appl Pharmacol 2008 : However, OTA caused a dose dependent reduction in LPS induced TF ( activity, antigen and mRNA ) and PAI-2 ( antigen and mRNA ) production with > 85 % inhibition at 1 mug/ml. Similar results were obtained when monocyte enriched preparations were used instead of MNC
Sekine et al., Mol Cell Biol 2009 (Shock, Septic) : Analysis of gene expression revealed that AhR directly regulates the expression of Pai-2 through a mechanism involving NF-kappaB but not AhR nuclear translocator (Arnt), in an LPS dependent manner
Udofa et al., PloS one 2013 : Lipopolysaccharide (LPS) , a potent bacterial endotoxin, can induce SerpinB2 expression via the toll-like receptor 4 (TLR4) by ~1000-fold over a period of 24 hrs in murine macrophages ... Importantly, both constitutive and LPS induced SerpinB2 expression was severely abrogated in C/EBP-ß-null mouse embryonic fibroblasts ( MEFs ) and primary C/EBP-ß-deficient peritoneal macrophages
Ritchie et al., Blood 1995 (Inflammation...) : Thrombin and lipopolysaccharide (LPS) stimulated comparable levels of PAI-2 , studied at the antigen and mRNA level
Eggesbø et al., Thromb Res 1995 (Hyperlipoproteinemias...) : Upon stimulation with LPS , PCA and released PAI-2 increased sharply, while PA and released uPA declined
Semeraro et al., J Infect Dis 1996 (Helicobacter Infections) : These findings suggest that the induction of monocyte tissue factor and PAI-2 by H. pylori LPS is influenced by the lipid A structure and modulated by the core oligosaccharide and that phosphate groups present in both regions may play an important role