ABSTRACT
NF-κB regulates the expression of Cyclin D1 (CD1), while RAC3 is an NF-κB coactivator that enhances its transcriptional activity. In this work, we investigated the regulatory role of CD1 on NF-κB activity. We found that CD1 inhibits NF-κB transcriptional activity through a corepressor function that can be reverted by over-expressing RAC3. In both, tumoral and non-tumoral cells, the expression pattern of RAC3 and CD1 is regulated by the cell cycle, showing a gap between the maximal expression levels of each protein. The individual increase, by transfection, of either CD1 or RAC3 enhances cell proliferation. However the simultaneous and constitutive over-expression of both proteins has an inhibitory effect. Our results suggest that the relative amounts of CD1 and RAC3, and the timing of expression of these oncogenes could tilt the balance of tumor cell proliferation in response to external signals.
Subject(s)
Co-Repressor Proteins/metabolism , Cyclin D1/metabolism , NF-kappa B/metabolism , Binding Sites , Cell Adhesion , Cell Cycle , Cell Line, Tumor , Cell Proliferation , DNA/metabolism , HEK293 Cells , Humans , Models, Biological , NF-kappa B/genetics , Protein Binding , Protein Transport , Transcription, Genetic , Transcriptional Activation/genetics , rac GTP-Binding Proteins/metabolismABSTRACT
Protein phosphatase type 2A (PP2A) activity is required for the sucrose induction of fructan metabolism in wheat leaves, as shown in experiments with the addition of the specific inhibitor okadaic acid (OA) together with sucrose. However, a decrease in total PP2A activity has been found along sucrose treatment. Here we analyze the effect of sucrose feeding to wheat leaves on PP2A activity profiles after Deae-Sephacel and Superose separation, in comparison with those of control leaves. The results show no evidence of changes in PP2A activity profiles as a consequence of sucrose feeding. In all, our data suggest that constitutive levels of PP2A activity may be sufficient for the sucrose-mediated induction of fructan metabolism and that general decrease of PP2A activity produced by long-term treatment with sucrose may be due to a negative feedback regulation.
