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ZEB2, initially identified as Smad interacting-protein 1, is normally located in the nucleus and functions as a DNA-binding transcriptional repressor that interacts with activated SMADs. Like the homologous ZEB1, ZEB2 inhibits the transcription of the E-cadherin gene and induces epithelial-mesenchymal transition, a genetic program controlling cell migration during embryonic development and wound healing, in vitro. ZEB2 can also protect cells from DNA damage-induced apoptosis, suggesting that its expression may contribute to tumor progression. Recent evidence has shown that ZEB2 is often observed in the cytoplasm in numerous cancer tissues, indicating that its localization may be regulated in normal and tumor tissues. Mutations in this gene are also associated with Hirschsprung disease/Mowat-Wilson syndrome.
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