p(MGI:"interleukin 1 alpha")
These experiments were performed in U373 glioma cells, which similarly to human and mouse astrocytes, upregulate expression of both YKL-40 and RelB in response to IL-1 and OSM, and this cytokine-induced expression is diminished by the knockdown of p50 and RelB (Suppl. Fig. 4). PubMed:25681350
These experiments were performed in U373 glioma cells, which similarly to human and mouse astrocytes, upregulate expression of both YKL-40 and RelB in response to IL-1 and OSM, and this cytokine-induced expression is diminished by the knockdown of p50 and RelB (Suppl. Fig. 4). PubMed:25681350
More importantly, OSM significantly enhanced IL-1-induced formation of the p50/RelB complexes PubMed:25681350
Constitutively active STAT3 enhanced, whereas dominant-negative IκBα diminished cytokine-responsiveness. PubMed:25681350
Constitutively active STAT3 enhanced, whereas dominant-negative IκBα diminished cytokine-responsiveness. PubMed:25681350
NF-κB and STAT3 are the major transcription factors activated by IL-1 and OSM, respectively PubMed:25681350
NF-κB and STAT3 are the major transcription factors activated by IL-1 and OSM, respectively PubMed:25681350
OSM and IL-1 efficiently regulated YKL-40 expression via STAT3 (Fig. 3A) and OSM promoted the recruitment of IL-1-induced p50 to the YKL-40 promoter (Fig. 5B). PubMed:25681350
Downregulation of STAT3 (Fig. 3C) dramatically diminished IL-1/OSM-induced YKL-40 mRNA expression (Fig. 3A). PubMed:25681350
Similarly, RelB mRNA expression was also up-regulated by IL-1 in mouse astrocytes (Fig. 4D). PubMed:25681350
These data suggests that RelB regulates expression of YKL-40 in response to proinflammatory cytokines, such as IL-1 and TNF, which induce canonical activation of RelB/p50 complexes. PubMed:25681350
These data suggests that RelB regulates expression of YKL-40 in response to proinflammatory cytokines, such as IL-1 and TNF, which induce canonical activation of RelB/p50 complexes. PubMed:25681350
Indeed, p50/RelB complexes were formed in response to IL-1 PubMed:25681350
More importantly, OSM significantly enhanced IL-1-induced formation of the p50/RelB complexes PubMed:25681350
These experiments were performed in U373 glioma cells, which similarly to human and mouse astrocytes, upregulate expression of both YKL-40 and RelB in response to IL-1 and OSM, and this cytokine-induced expression is diminished by the knockdown of p50 and RelB (Suppl. Fig. 4). PubMed:25681350
In agreement with the mutational analysis that showed the importance of the proximal NF-κB site (Fig. 3D), strong protein binding to the proximal, but not distal, NF-κB site of the YKL-40 promoter was induced by IL-1 alone or together with OSM (Fig. 5C). PubMed:25681350
OSM and IL-1 efficiently regulated YKL-40 expression via STAT3 (Fig. 3A) and OSM promoted the recruitment of IL-1-induced p50 to the YKL-40 promoter (Fig. 5B). PubMed:25681350
OSM and IL-1 efficiently regulated YKL-40 expression via STAT3 (Fig. 3A) and OSM promoted the recruitment of IL-1-induced p50 to the YKL-40 promoter (Fig. 5B). PubMed:25681350
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.