p(MGI:"chitinase-like 1")

Entity

Name

chitinase-like 1

Namespace

mgi

Namespace Version

20190224

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/c328ad964c08967a0417a887510b97b965a62fa5/external/mgi-names.belns

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. 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

Cumulatively, these data suggest that in cells expressing relatively low levels of YKL-40, such as astrocytes, cytokine-driven RelB promotes YKL-40 induction in vitro and in vivo. PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. PubMed:25681350

Although RelB and p50 did not bind to the YKL-40 promoter in unstimulated U373 cells, binding of RelB and p50 was apparent in cytokine-treated cells (Fig. 5B), suggesting that RelB/p50 complexes directly regulate YKL-40 expression. PubMed:25681350

We conclude that RelB/p50 complexes can directly bind to the proximal NF-κB site of the YKL-40 promoter and are essential for the cytokine-induced YKL-40 expression. 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

These data suggest that in addition to STAT3 activation, OSM enhances YKL-40 expression by promoting formation of the RelB/p50 complexes, which bind to the YKL-40 promoter PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. PubMed:25681350

Since p65 subunit of NF-κB and STAT3 were previously implicated in cytokine-induced expression of YKL-40 (8, 34), we knocked down their expression in human astrocytes 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

Since p65 subunit of NF-κB and STAT3 were previously implicated in cytokine-induced expression of YKL-40 (8, 34), we knocked down their expression in human astrocytes PubMed:25681350

Surprisingly, knockdown of p65 had no effect on YKL-40 mRNA expression (Fig. 3A), but did drastically diminish the expression of IL-8 mRNA, which is p65-dependent (Fig. 3B). PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. 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

Since p65 subunit of NF-κB and STAT3 were previously implicated in cytokine-induced expression of YKL-40 (8, 34), we knocked down their expression in human astrocytes PubMed:25681350

Surprisingly, knockdown of p65 had no effect on YKL-40 mRNA expression (Fig. 3A), but did drastically diminish the expression of IL-8 mRNA, which is p65-dependent (Fig. 3B). PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. PubMed:25681350

Since p65 subunit of NF-κB and STAT3 were previously implicated in cytokine-induced expression of YKL-40 (8, 34), we knocked down their expression in human astrocytes PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. PubMed:25681350

Knockdown of either RelB or p50 significantly diminished cytokine-induced YKL-40 mRNA expression, whereas knockdown of p65, cRel and p52 had no effect (Fig. 4A). This finding implicates both RelB and p50 in YKL-40 regulation. PubMed:25681350

Cytokine stimulation facilitated the binding of protein complexes to the proximal NF-κB element in vitro, which super-shifted with anti-p65, anti-RelB and anti-p50 antibodies (Fig. 5D), indicating that the proximal NF-κB site can bind both p65/p50 and RelB/p50 complexes. PubMed:25681350

Cytokine stimulation facilitated the binding of protein complexes to the proximal NF-κB element in vitro, which super-shifted with anti-p65, anti-RelB and anti-p50 antibodies (Fig. 5D), indicating that the proximal NF-κB site can bind both p65/p50 and RelB/p50 complexes. PubMed:25681350