Recruitment of RelB to the Csf2 promoter enhances RelA-mediated transcription of granulocyte-macrophage colony-stimulating factor.
Ontology highlight
ABSTRACT: Tumor necrosis factor (TNF) induces expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) but lymphotoxin β (LTβ) does not. Here we report that priming of cells with agonistic LTβ receptor antibody synergistically enhanced TNF-induced GM-CSF expression. The LTβ priming process was not due to an increase in TNF-mediated nuclear translocation of p65, p65 DNA binding, or NF-κB transactivational activity. The synergistic effect of LTβ priming was not observed with other TNF-responsive genes such as Ccl2 or RelB, which suggested that this effect was not a general increase in TNF signaling. Furthermore, RelB and p65 were both independently recruited to the GM-CSF promoter when cells were primed with LTβ followed by TNF treatment. As a consequence, an increase in both chromatin
SUBMITTER: Sasaki CY
PROVIDER: S-EPMC3020716 | biostudies-literature | 2011 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA