Gene interactions and pathways from curated databases and text-mining

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IL6 — SAA1

Text-mined interactions from Literome

Nguyen et al., J Biol Chem 1999 : Treatment of primary rat hepatocytes or tranfected HepG2 cells with the alpha ( 1B ) -adrenergic receptor ( alpha ( 1B ) AR ) agonist phenylephrine ( PE ) significantly inhibited interleukin 6 (IL-6) induced STAT3 binding, tyrosine phosphorylation, and IL-6 induced serum amyloid A mRNA expression
Sasaki et al., J Med Microbiol 2001 (Streptococcal Infections) : Furthermore, a reverse transcription-PCR assay revealed that SAA 10 microg/ml could induce mRNA accumulation of tumour necrosis factor-alpha, interleukin (IL)-1beta and IL-6 as well as iNOS
Hayashi et al., Proc Natl Acad Sci U S A 2002 (Bone Resorption) : Not only did MDL-A markedly inhibit IL-6- and IL-11 induced osteoclastogenesis in vitro, but it also inhibited IL-6 stimulated serum amyloid A production and bone resorption in an experimental model of postmenopausal osteoporosis in vivo by a different mechanism from that of 17beta-estradiol
Thorn et al., Amyloid 2002 : The Saa1 and Saa2 promoters are strongly induced by IL-6 , with synergistic upregulation of Saa2, but not of Saa1, by IL-1 or TNF
Ribeiro et al., Mediators Inflamm 2003 : In a previous study, we reported that SAA induces the release of tumor necrosis factor-alpha, interleukin (IL)-1beta and IL-8 from human blood neutrophils
Ganapathi et al., Biochem J 1992 (Carcinoma, Hepatocellular...) : Okadaic acid ( OA ), a specific inhibitor of protein phosphatases 1 and 2A, inhibited in a dose dependent manner ( 5-20 nM ) the induction of C-reactive protein (CRP), serum amyloid A (SAA) and fibrinogen by interleukin-6 (IL-6) plus interleukin-1 (IL-1), and of fibrinogen by IL-6 alone, in Hep 3B cells
Hagihara et al., Biochem Biophys Res Commun 2004 : IL-6 plays a critical role in the synergistic induction of human serum amyloid A (SAA) gene when stimulated with proinflammatory cytokines as analyzed with an SAA isoform real-time quantitative RT-PCR assay system ... Either IL-6 and IL-1beta or IL-6 and TNFalpha, but not IL-1beta and TNFalpha, induced the synergistic induction of SAA1 and SAA2 genes
Gervois et al., J Biol Chem 2004 (Acute-Phase Reaction) : PPARalpha prevents the IL-6 induced expression of the positive APR genes fibrinogen-alpha, -beta, -gamma, haptoglobulin, and serum amyloid A and the IL-6 induced suppression of the negative APR gene, major urinary protein
Thorn et al., Scand J Immunol 2004 : Here, we examine the roles of TNF-alpha, interleukin-6 (IL-6) and GCs on the transcriptional regulation of the two human A-SAA genes ( SAA1 and SAA2 ) and show that these stimuli have different effects on the SAA1 and SAA2 promoters in HepG2 hepatoma and KB epithelial cell lines
Ganapathi et al., J Immunol 1991 (Carcinoma, Hepatocellular...) : Similar results were obtained for the effect of dexamethasone on the induction of SAA by IL-6 plus IL-1 alpha
Kuzuhara et al., Eur J Pharmacol 2006 (Liver Failure) : We examined whether the 22beta-methoxyolean-12-ene-3beta,24 ( 4beta ) -diol ( ME3738 ) -mediated selective induction of interleukin-6 increased alpha1-acid glycoprotein and serum amyloid A expression, and whether these proteins protected against liver injury in vitro and in vivo
Pietrangelo et al., Gastroenterology 2007 : IL-6 stimulated phospho STAT3, serum amyloid A (SAA) , and suppressor of cytokine signaling 3 ( SOCS3 ) expression in livers of wild-type and alfpCregp130 ( Y757F/LoxP ) mice, whereas this response was blocked in alfpCre gp130 ( LoxP/LoxP ) and alfpCre gp130 ( DeltaSTAT/LoxP ) mice
Sipe et al., J Immunol 1992 (Acute-Phase Reaction) : Because neither tenidap nor naproxen inhibited SAA synthesis by cytokine stimulated Hep3B cells and because they differ most significantly in their effect on IL-6 production, the results support a role for IL-6 in the continued stimulation of SAA production during RA
Dowton et al., Pediatr Res 1991 (Acute-Phase Reaction) : Studies of immature hamsters after birth show that the responses of CRP and SAA genes to lipopolysaccharide, tumor necrosis factor, IL-1, and IL-6 are reduced when compared with induction of mRNA accumulation for these acute phase reactants in adult animals
Koga et al., FEBS Lett 2008 (Arthritis, Rheumatoid) : In this study, we investigated the role of serum amyloid A protein (SAA) in the production of interleukin-6 (IL-6) using rheumatoid arthritis fibroblast-like synoviocytes ( RA-FLS ) ... Inhibitor studies have shown SAA induced IL-6 production to be down-regulated by NF-kappaB inhibition and partially inhibited by p38 or JNK inhibitors ... Our findings demonstrate that SAA is a significant inducer of IL-6 , which is critically involved in RA pathogenesis
Yap et al., Biochim Biophys Acta 1991 : It inhibits also the stimulatory effect of IL-1 and IL-6 on the synthesis of CRP and SAA ... ( 3 ) Since anti-TNF enhances the stimulatory effect of IL-6 on the synthesis of CRP and SAA , it seems likely that TNF is also produced by the human hepatocytes
Wallerstedt et al., Diabetologia 2010 (Inflammation) : Consequently, nuclear translocation of STAT3 and the IL-6 induced gene transcription and protein release of the inflammatory molecule serum amyloid A 3 (SAA3) were reduced
Mullan et al., Am J Pathol 2010 (Arthritis, Rheumatoid...) : A-SAA induced interleukin-6 and -8 production was inhibited in the presence of anti-SR-B1 in human microvascular endothelial cells and RA FLCs
Nerstedt et al., Diabetologia 2010 : AICAR and metformin markedly blunt the IL-6 stimulated expression of SAA cluster genes as well as of haptoglobin in a dose dependent manner
Rienhoff et al., Mol Biol Med 1990 (Amyloidosis...) : Studies in vitro and in vivo demonstrated that the expression of SAA genes is regulated by the inflammatory cytokine interleukin-1 ... Moreover, both the interleukin-1 induced expression and the enhanced liver-specific expression of the SAA gene are controlled by the binding of nuclear proteins to specific DNA sequences upstream from the structural gene
Bauzá et al., J Surg Res 2012 (Acute-Phase Reaction...) : Serum IL-6 levels peaked at 3 h and fibrinogen-? and SAA mRNA levels increased more than 6-fold at 12 h before returning to control levels at 48 h
Migita et al., J Rheumatol 2011 (Acute-Phase Reaction...) : CP690,550 abrogated IL-6 mediated A-SAA mRNA expression in RA-FLS ... Similarly, CP690,550 inhibited IL-6 mediated A-SAA mRNA expression in human hepatocytes ... Our data indicated that CP690,550 blocked IL-6 induced JAK2/STAT3 activation, as well as the induction of A-SAA
Dong et al., Mol Med 2011 (Atherosclerosis...) : With increased SAA levels, the plasma levels of interleukin-6 and tumor necrosis factor-a were significantly increased
Pini et al., Cytokine 2013 (Endotoxemia...) : Hepatic induction of the acute-phase protein SAA by LPS was not affected by obesity or IL-6 deficiency, although baseline levels were highest in WT DIO mice
Anthony et al., Am J Respir Crit Care Med 2013 (Disease Models, Animal...) : SAA predominately promoted expression of the TH17 polarizing cytokine IL-6 , which was opposed by 15-epi-lipoxin A4, a counter-regulatory mediator, and ALX/FPR2 ligand
Mackiewicz et al., Biochem J 1988 : Comparison of these findings with those in human hepatoma cell lines, in which interleukin-1 does not induce serum amyloid A synthesis, suggests that the effect of interleukin-1 on serum amyloid A synthesis may be indirect
Weinstein et al., J Trauma 1987 (Acute-Phase Reaction...) : The effect of interleukin-1 on mouse liver serum amyloid A mRNA levels was investigated
Moshage et al., Biochem Biophys Res Commun 1988 : The effect of interleukin-1 , interleukin-6 and its interrelationship on the synthesis of serum amyloid A and C-reactive protein in primary cultures of adult human hepatocytes ... These findings suggest that IL-6 plays a key role in the stimulation of synthesis of serum amyloid A and C-reactive protein by the human liver cells
Conti et al., Immunol Invest 1995 (Carcinoma, Hepatocellular) : Synergistic activation of serum amyloid A (SAA) by IL-6 and IL-1 in combination on human Hep 3B hepatoma cell line
Jiang et al., J Immunol 1995 : Induction of human serum amyloid A in Hep 3B cells by IL-6 and IL-1 beta involves both transcriptional and post-transcriptional mechanisms
Steel et al., Biochem J 1993 (Carcinoma, Hepatocellular...) : These data provide evidence of a paradox with regard to the transcriptional upregulation of A-SAA by IL-1 beta + IL-6 and the relative synthesis of A-SAA protein and suggest a role for post-transcriptional control of A-SAA biosynthesis during the acute phase
Shimetani et al., Nihon Rinsho Meneki Gakkai Kaishi 1997 (Liver Neoplasms, Experimental) : A cytokine IL-6 induced the CRP production in the presence of IL-1 beta, but did not affect the constitutive production of SAA
Lozanski et al., Biochem J 1997 (Carcinoma, Hepatocellular) : The ability of C2 and C6 to potentiate the effects of cytokines suggests that the sphingomyelin-ceramide pathway participates in induction of CRP and SAA by IL-6+IL-1beta under these experimental conditions, most likely by transducing the effects of IL-1beta ... C2 and C6 were unable to substitute for IL-1beta in enhancing IL-6 effects on CRP and SAA , consistent with other reports indicating that the sphingomyelin-ceramide pathway is only a single component of multiple necessary converging pathways for induction of many genes
Foyn Bruun et al., Clin Exp Immunol 1998 : In contrast to what has been shown in previous in vivo studies, administration of IL-6 did increase the SAA levels to nearly the same magnitude as IL-1, and the effect of IL-6 and LPS on SAA production was not significantly altered by the addition of DEX
Benigni et al., Am J Pathol 1998 : On the other hand, administration of murine NGF did not elevate serum corticosterone or IL-6 , but induced SAA
Ray et al., J Biol Chem 1999 : We demonstrate that SAA is synergistically induced in synovial cells by interleukin (IL)-1 and IL-6 that are present at significantly high level in the synovial fluid of arthritis patients ... Mutation of these sequences abolishes SAA promoter response to IL-1 and IL-6