Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-kappa B.

摘要: NF-κB, which consists of two polypeptides, p50 (Mr 50K) and p65/RelA 65K), is thought to be a key regulator genes involved in responses infection, inflammation stress1. Indeed, although developmentally normal, mice deficient display functional defects immune responses2. Here we describe the generation RelA subunit NF-κB. Disruption relA locus leads embryonic lethality at 15–16 days gestation, concomitant with massive degeneration liver by programmed cell death or apoptosis. Embryonic fibroblasts from RelA-deficient are defective tumour necrosis factor (TNF)-mediated induction messenger RNAs for IκBα granulocyte/macrophage colony stimulating (GM-CSF), basal levels these transcripts unaltered. These results indicate that controls inducible, but not basal, transcription NF-κB-regulated pathways.