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B
Overexpression Delays Tumor Formation in v-rel
Transgenic Mice
By
From the Department of Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute,
Princeton, New Jersey 08543-4000
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 
B-binding activity. Since experimental evidence has led to the suggestion of a potential tumor suppressor activity for IB
,
we have studied the role of IB in the transforming activity of v-Rel by overexpressing IB in v-rel transgenic mice. Overexpression of IB 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 IB may be a key element in its transforming capability.
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