Abstract
RATIONALE: IL-4 and IL-13 activate signaling cascades leading to activation of the transcription factor Stat6, which acts as a critical mediator of Th2 inflammation. We have demonstrated that cycling of Stat6 between the nucleus and cytoplasm is essential to maintaining Stat6 responses. Others have demonstrated that Stat1 and Stat3 utilize CRM1 association with leucine-rich target regions to mediate nuclear export. We investigated homologous leucine-rich regions in Stat6 and other key structural elements to determine the mechanism of Stat6 nuclear export.
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