ELAV proteins are implicated in regulating the stability and translation of 
cytokine and growth regulatory mRNAs such as GM-CSF, IL-2, c-myc, c-fos and 
GLUT1 by binding to their AU-rich 3'UTRs. The tissue-specific ELAV protein HuB 
(aka. Hel-N1) is predominantly cytoplasmic and has been shown to stabilize GLUT1 
and c-myc mRNAs and to increase their translation following ectopic expression 
in 3T3-L1 cells. We report that the most widely expressed mouse ELAV protein, 
mHuA, is predominately nuclear in cultured NIH-3T3 cells, but is localized in 
the cytoplasm during early G1 of the cell cycle. Therefore, much like the 
primarily cytoplasmic HuB, HuA becomes temporally localized in the cytoplasm 
where it can potentially regulate the stability or translation of bound mRNAs. 
Moreover, we report that stimulation of mouse spleen cells using either 
mitogenic or sub-mitogenic levels of anti-CD3/CD28 resulted in a dramatic 
increase in the level of HuA. Upregulation of HuA corresponds to previously 
documented increases in cytokine expression which are due to increased mRNA 
stability following T cell activation. Consistent with these findings, HuA was 
down regulated in quiescent cells and upregulated in 3T3 cells following serum 
stimulation. The increase of murine HuA during the cell cycle closely resembles 
that of cyclin B1 which peaks in G2/M. Together with our earlier studies, these 
data indicate that mammalian ELAV proteins function during cell growth and 
differentiation due in part to their effects on posttranscriptional stability 
and translation of multiple growth regulatory mRNAs. This supports the 
hypothesis that ELAV proteins can function as transacting factors which affect a 
default pathway of mRNA degradation involved in the expression of growth 
regulatory proteins.