| First Author | Zhang JY | Year | 2004 |
| Journal | Genes Dev | Volume | 18 |
| Issue | 1 | Pages | 17-22 |
| PubMed ID | 14724177 | Mgi Jnum | J:119420 |
| Mgi Id | MGI:3702201 | Doi | 10.1101/gad.1160904 |
| Citation | Zhang JY, et al. (2004) NF-kappaB RelA opposes epidermal proliferation driven by TNFR1 and JNK. Genes Dev 18(1):17-22 |
| abstractText | 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. |
