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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Zhang, JY; Green, CL; Tao, S; Khavari, PA

Published Date

  • January 1, 2004

Published In

Volume / Issue

  • 18 / 1

Start / End Page

  • 17 - 22

PubMed ID

  • 14724177

Pubmed Central ID

  • PMC314269

International Standard Serial Number (ISSN)

  • 0890-9369

Digital Object Identifier (DOI)

  • 10.1101/gad.1160904


  • eng

Conference Location

  • United States