Journal
GENES & DEVELOPMENT
Volume 18, Issue 1, Pages 17-22Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1160904
Keywords
epidermis; NF-kappa B; proliferation; differentiation
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Funding
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR043799, R29AR043799, R01AR045192] Funding Source: NIH RePORTER
- NIAMS NIH HHS [R01 AR043799, R01 AR045192, AR43799, AR45192] Funding Source: Medline
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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. RBlA(-/-) epidermis displays hyperplasia without abnormal differentiation, inflammation, or apoptosis. Hyperproliferation is TNFR1-dependent because Tnfr1 deletion normalized cell division. TNFR1-dependent INK activation occurred in RelA(-/-) epidermis, and INK 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.
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