Abstract
Regulating maf1 expression and its expanding biological functions.
Highlights
Studies on Maf1 regulation up until now have focused on posttranslational mechanisms, notably phosphorylation, which controls Maf1 localization and its interaction with the polymerase [2,3]
Tissue-specific PTEN knockout mice and a human PTEN null mutant cell line with inducible PTEN expression were used to perturb PI3K/ AKT/FoxO1 signaling and show that Maf1 expression can be varied in both directions
Mouse embryo fibroblasts in which the AKT substrate FoxO1 was knocked down or constitutively active showed reduced and elevated Maf1 protein levels, respectively, with corresponding reciprocal effects on the levels of precursor tRNAs
Summary
Studies on Maf1 regulation up until now have focused on posttranslational mechanisms, notably phosphorylation, which controls Maf1 localization (in yeast) and its interaction with the polymerase (in yeast and humans) [2,3]. The new work from Palian and colleagues shows that the steady-state level of the Maf1 protein is regulated. This is achieved through PI3K/AKT/FoxO1 signaling (Fig. 1).
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