Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
avian reticuloendotheliosis viral (v-rel) oncogene related B
Namespace
mgi
Namespace Version
20190224
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/c328ad964c08967a0417a887510b97b965a62fa5/external/mgi-names.belns

Appears in Networks 1

In-Edges 5

p(MGI:"interleukin 1 alpha") increases act(p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B")) View Subject | View Object

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

p(MGI:"tumor necrosis factor") increases act(p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B")) View Subject | View Object

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

path(MESH:Glioblastoma) increases p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") View Subject | View Object

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

Out-Edges 6

p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") increases r(MGI:"chitinase-like 1") View Subject | View Object

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

p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") regulates p(MGI:"chitinase-like 1") View Subject | View Object

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

p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") regulates p(MGI:"chitinase-like 1") View Subject | View Object

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

p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") increases p(MGI:"chitinase-like 1") View Subject | View Object

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

p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") increases act(p(MGI:"interleukin 1 alpha")) View Subject | View Object

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

p(MGI:"avian reticuloendotheliosis viral (v-rel) oncogene related B") increases act(p(MGI:"oncostatin M")) View Subject | View Object

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

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.