Our findings show that the same site on IBD is involved in binding to MLL and HIV-IN, revealing an attractive approach to simultaneously target LEDGF in leukemia and HIV.
In this issue, Yokoyama and Cleary (2008) show that menin's essential, and perhaps only, contribution to leukemia is to tether a third protein, LEDGF--a chromatin-associated protein implicated in leukemia and several other disease states--to MLL.
We demonstrate here that these discordant functions are unified by menin's ability to serve as a molecular adaptor that physically links the MLL (mixed-lineage leukemia) histone methyltransferase with LEDGF (lens epithelium-derived growth factor), a chromatin-associated protein previously implicated in leukemia, autoimmunity, and HIV-1 pathogenesis.