Differential RelA- and RelB-dependent gene transcription in LTbetaR-stimulated mouse embryonic fibroblasts.

ABSTRACT:

Background

Lymphotoxin signaling via the lymphotoxin-beta receptor (LTbetaR) has been implicated in biological processes ranging from development of secondary lymphoid organs, maintenance of spleen architecture, host defense against pathogens, autoimmunity, and lipid homeostasis. The major transcription factor that is activated by LTbetaR crosslinking is NF-kappaB. Two signaling pathways have been described, the classical inhibitor of NF-kappaB alpha (IkappaBalpha)-regulated and the alternative p100-regulated pathway that result in the activation of p50-RelA and p52-RelB NF-kappaB heterodimers, respectively.

Results

Using microarray analysis, we investigated the transcriptional response downstream of the LTbetaR in mouse embryonic fibroblasts (MEFs) and its regulation by the

SUBMITTER: Lovas A 

PROVIDER: S-EPMC2637282 | biostudies-literature | 2008 Dec

REPOSITORIES: biostudies-literature