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Genes Dev. 2004 Jan 1;18(1):17-22.

NF-kappaB RelA opposes epidermal proliferation driven by TNFR1 and JNK.

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1
VA Palo Alto Healthcare System, Palo Alto, California 94305, USA.

Erratum in

  • Genes Dev. 2004 Feb 15;18(4):461.

Abstract

NF-kappaB inhibition promotes epidermal tumorigenesis; however, whether this reflects an underlying role in homeostasis or a special case confined to neoplasia is unknown. Embryonic lethality of mice lacking NF-kappaB RelA has hindered efforts to address this. We therefore generated developmentally mature RelA(-/-) skin. RelA(-/-) epidermis displays hyperplasia without abnormal differentiation, inflammation, or apoptosis. Hyperproliferation is TNFR1-dependent because Tnfr1 deletion normalized cell division. TNFR1-dependent JNK activation occurred in RelA(-/-) epidermis, and JNK inhibition abolished hyperproliferation due to RelA deficiency. Thus, RelA antagonizes TNFR1-JNK proliferative signals in epidermis and plays a nonredundant role in restraining epidermal growth.

PMID:
14724177
PMCID:
PMC314269
DOI:
10.1101/gad.1160904
[Indexed for MEDLINE]
Free PMC Article
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