Gene interactions and pathways from curated databases and text-mining

◀ Back to IL6

IL6 — IRF1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Coccia et al., J Biol Chem 1999 : No significant differences of IRF-1 mRNA expression were found in established Th1 and Th2 cells ; however, interleukin 12 (IL-12) induced a strong up-regulation of IRF-1 transcripts in Th1 but not in Th2 cells
Samardzic et al., Cytokine 2001 : These results indicate that STAT1 activation and subsequent IRF-1 transcription are required for induction of iNOS, but not IL-6 in murine fibroblasts
Colombatti et al., Glia 2001 (Multiple Sclerosis) : We found that T-cell adhesion and T-cell soluble factors induce IL-6 gene expression in U251 astrocytes through distinct signaling pathways, respectively, resulting in the activation of NF-kappaB and IRF-1 transcription factors
Tsung et al., Am J Physiol Gastrointest Liver Physiol 2006 (Reperfusion Injury) : IL-6 and lipopolysaccharide had no effect on IRF-1 expression
Abdollahi et al., Cell Growth Differ 1991 : Using a clone of M1 cells inducible for terminal differentiation by both interleukin 6 (IL-6) and leukemia inhibitory factor (LIF), two multifunctional cytokines recently identified as physiological inducers of hemopoietic cell differentiation, it has been shown that IRF-1 expression is rapidly induced by IL-6 and LIF in the absence of protein synthesis and is followed by a later increase in the levels of IFN-beta mRNA, observed to be largely dependent on protein synthesis ... Taken together, these findings imply a regulatory cascade, where induction of terminal myeloid differentiation by IL-6 or LIF triggers the immediate early activation of IRF-1 , leading to the later induction of IFN-beta, in turn playing an autocrine role in growth inhibition
Mudter et al., Inflamm Bowel Dis 2011 (Colitis...) : In contrast to DSS colitis, IRF4 deficiency was protective in T-cell dependent transfer colitis associated with reduced RORa/?t levels and impaired IL-6 , IL-17a, and IL-22 production, suggesting that IRF4 acts as a master regulator of mucosal Th17 cell differentiation
Sancéau et al., J Biol Chem 1995 : Triggering of the human interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B, and Sp1 transcription factors ... Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha, in monocytic cells, involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter
Harroch et al., EMBO J 1994 (Breast Neoplasms...) : Induction by interleukin-6 of interferon regulatory factor 1 (IRF-1) gene expression through the palindromic interferon response element pIRE and cell type dependent control of IRF-1 binding to DNA ... The effects of interleukin-6 (IL-6) on interferon regulatory factor 1 (IRF-1) gene expression were studied in B-hybridoma B9 cells which are growth stimulated by IL-6 and breast carcinoma T47D cells which are growth inhibited ... IL-6 induced the production of IRF-1 mRNA and protein in both cell types, but IRF-1 binding activity to its target DNA sequence was induced only in T47D cells
Harroch et al., J Biol Chem 1993 : The dissociation between induction of mRNAs and of protein binding observed suggests that the activity of the IRF proteins is regulated by IL-6
Fontaine et al., Melanoma Res 1998 (Melanoma) : However, in contrast to IFNgamma, IL-6 triggered lower IRF-1 DNA binding activity and induced barely detectable IRF-1 dependent transactivation activity
Choi et al., Immunol Lett 1998 : Interferon regulatory factor-1 (IRF-1) is a transcription factor on the enhancer of type I interferons, and its gene expression is induced by IL-6 ... In addition, co-transfection of protein phosphatase 2A (PP2A) antisense constructs further increased IL-6 induced IRF-1 promoter activity, suggesting that PP2A is involved in IL-6 signaling