| First Author | Carrasco D | Year | 1997 |
| Journal | J Exp Med | Volume | 186 |
| Issue | 2 | Pages | 279-88 |
| PubMed ID | 9221757 | Mgi Jnum | J:41756 |
| Mgi Id | MGI:894441 | Doi | 10.1084/jem.186.2.279 |
| Citation | Carrasco D, et al. (1997) IkappaBalpha overexpression delays tumor formation in v-rel transgenic mice. J Exp Med 186(2):279-88 |
| abstractText | We have previously shown that transgenic mice expressing the oncoprotein v-Rel under the control of a T cell-specific promoter develop T cell lymphomas. Tumor formation was correlated with the presence of p50/v-Rel and v-Rel/v-Rel nuclear kappaB-binding activity. Since experimental evidence has led to the suggestion of a potential tumor suppressor activity for IkappaBalpha, we have studied the role of IkappaBalpha in the transforming activity of v-Rel by overexpressing IkappaBalpha in v-rel transgenic mice. Overexpression of IkappaBalpha in v-rel transgenic mice resulted in an extended survival, and the development of cutaneous T cell lymphomas of CD8(+)CD4(-) phenotype. These phenotypic alterations were associated with a dramatic reduction of p50/v-Rel, but not v-Rel/v-Rel nuclear DNA binding activity and an increased expression of the intercellular adhesion molecule 1. Our results indicate that v-Rel homodimers are active in transformation and that the capacity of v-Rel-containing complexes to escape the inhibitory effect of IkappaBalpha may be a key element in its transforming capability. |
