Conclusions

Our work on the Drosophila IDGFs supports the idea that the mammalian relatives might contribute to inflammatory disease by acting as mitogens on fibroblasts and perhaps other cell types. If confirmed, this finding opens up major new opportunities for rational drug design for some common and debilitating disorders. As far as we are aware, none of the mammalian proteins has been tested for any interaction with the insulin pathway. The identification and analysis of the IDGFs should help in understanding the functions of these mammalian family members and their relationships to disease states.

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