Gene interactions and pathways from curated databases and text-mining

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IL1A — LCN2

Text-mined interactions from Literome

Sommer et al., J Cell Biochem 2009 : In the current study, we determined regulation of Lcn2 by the proinflammatory and insulin resistance inducing cytokine interleukin (IL)-1beta in 3T3-L1 and brown adipocytes by relative real-time reverse transcription-polymerase chain reaction
Hiroshima et al., Arch Oral Biol 2011 : Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1a ( inducible AMPs ) ; the other AMPs were considered to be constitutive
Arena et al., Mediators Inflamm 2010 (Kidney Failure, Chronic) : Both IL-1ß and TNF-a regulate NGAL expression in polymorphonuclear granulocytes of chronic hemodialysis patients
Tadesse et al., Reprod Sci 2011 (Chorioamnionitis...) : IL-1ß , TNF-a, and LPS stimulated NGAL in cytotrophoblast cells ( not syncytiotrophoblast and decidua ) in vitro
Sugihara et al., Radiat Res 2013 : Based on microarray analysis of molecular pathways, we predicted that the enhanced gene expression of Lcn2 in MEFs might be caused by interleukin-1 (IL-1) in the serum of the irradiated mice, and that an IL-1a antibody could completely neutralize the enhanced gene expression of Lcn2 in MEFs
Chang et al., Biochem Biophys Res Commun 2013 : IL-1ß significantly induced LCN-2 expression while IFN-? alone did not induce it ... However, promoter study and EMSA showed that IFN-? failed to potentiate IL-1ß induced LCN-2 promoter activity and binding activity of transcription factors on LCN-2 promoter ... Furthermore, LCN-2 mRNA stability and transcription factors NF-?B and STAT-1 were not involved in the stimulatory effect of IFN-? on IL-1ß induced LCN-2 expression ... Meanwhile, Western Blot and promoter analyses showed that NF-?B was a key factor in IL-1ß induced LCN-2 expression ... Collectively, IL-1ß induces LCN-2 expression via NF-?B activation in RINm5F ß-cells ... IFN-? potentiates IL-1ß induced LCN-2 expression at mRNA and protein levels, but not at promoter level and the stimulatory effect of IFN-? is independent of NF-?B and STAT-1 activation