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IL1B — TCF15

Text-mined interactions from Literome

Tolando et al., Free Radic Biol Med 2000 : Because Se supplementation decreases cytokine induced NF-kappaB activity, whereas added H ( 2 ) O ( 2 ) is inactive and catalase does not affect the activation induced by TNF-alpha, it is concluded that only intracellularly generated H ( 2 ) O ( 2 ) has a role in transcription factor activation by both TNF-alpha and IL-1beta
Brzoska et al., Ann N Y Acad Sci 1999 : Since the molecular basis of these antiinflammatory effects is not well known, the influence of alpha-MSH on IL-1 beta induced chemokine production and transcription factor activation was investigated in human keratinocytes
Frost et al., Endocrinology 2000 : The transcription factor CREB, a potential substrate of both protein kinase A (PKA) and RSK-1, is phosphorylated in response to IL-1beta and cAMP in HepG2 cells
Terzidou et al., J Clin Endocrinol Metab 2006 : OTR promoter contains putative transcription factor binding sites for activating protein-1 (AP-1), CCAAT/enhancer binding protein (C/EBP), and nuclear factor-kappaB (NF-kappaB), which may be activated by IL-1beta , whose concentrations increase with labor
Zaragoza et al., Biol Reprod 2006 : The interleukin 1beta induced expression of human prostaglandin F2alpha receptor messenger RNA in human myometrial derived ULTR cells requires the transcription factor , NFkappaB
Peng et al., J Cell Physiol 2008 : The epithelium-specific ETS (ESE)-1 transcription factor is induced in chondrocytes by interleukin-1beta (IL-1beta)
Liu et al., Cell Biol Int 2009 (Acute Lung Injury...) : Our results revealed that IL-1beta induced PBEF expression in pulmonary vascular endothelial cells at the transcriptional level and a -1535 T-variant in the human PBEF gene promoter significantly attenuated its binding to an IL-1beta induced unknown transcription factor
Bonizzi et al., J Immunol 1997 : We previously demonstrated that IL-1beta mediated induction of the nuclear factor-kappaB (NF-kappaB) transcription factor proceeds through the production of reactive oxygen intermediates in lymphoid cells, while it occurs independently of any oxidative stress in epithelial transformed cells
Wang et al., Invest Ophthalmol Vis Sci 1999 : To determine whether nuclear transcription factor-kappaB ( NF-kappaB ) is activated in human retinal pigment epithelial ( hRPE ) cells in response to interleukin-1beta (IL-1beta) , tumor necrosis factor-alpha (TNF-alpha), or interferon-gamma (IFN-gamma) alone or in combination and if so, whether expression of proinflammatory genes induced by these agents can be blocked by a proteasome inhibitor, MG-132, which inhibits the degradation of I kappaB, an NF-kappaB inhibitor, thereby preventing nuclear translocation of NF-kappaB