Functional analysis of the mouse Jmjd6 gene
Funded by: Previously funded by the German Research Council (DFG)
The mouse jumonji domain containing gene 6 (Jmjd6) belongs to the superfamily of JmjC-domain containing metalloenzymes which are involved in oxidative protein modifications. Previously described as a phosphatidylserine receptor for the phagocytosis apoptotic cells it has now become clear that Jmjd6 functions as a nuclear protein.
A few years ago we generated Jmjd6 knockout mice and showed that the gene is essential for cellular differentiation and development (Böse et al., 2004; Schneider et al., 2004). In addition, Jmjd6-deficient macrophages were found to be impaired in their capability to respond to microbial products.
In collaboration with the groups of Christopher Schofield (University of Oxford) and Angelika Böttger (Ludwig-Maximilians-University, Munich, Munich) we recently demonstrated that Jmjd6 hydroxylates the splicing proteins U2AF65 and LUC7L2 (Webby et al., 2009). We now want to understand how Jmjd6 regulates alternative splicing under oxygen limiting conditions. Of special interest to us are transcriptional responses of macrophages to hypoxic conditions during infection and inflammation.
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