Immune deviation, tissue degeneration and cancer are complex pathological processes that rely on the aberrant gene expression programs. Identifying those particulate "pathologic gene expression networks", that support the altered biosynthesis of molecules driving inflammation, autoimmunity, tissue damage and cancer may narrow down our selection for therapeutic targets and provide efficient cues of therapeutic intervention. Post-transcriptional gene regulation is currently emerging as a major target for pathological gene expression. In eukaryotic cells, the properties of mRNA stability and translational processing (a) are under tight control by cis-mRNA-elements and trans-acting protein factors; (b) respond rapidly to stimulation from the local microenvironment (c) define the time and the extent of protein-synthesis as to prevent aberrant production of potentially hazardous mediators. Failure to regulate a post-transcriptional process, either through the persistence of an inciting stimulus (stress, chemicals, mitogens) or a permutation of the modulating machinery (RNA binding proteins, signalling intermediates or cis elements), may provide the impetus for the development of disease. Our group is focusing on the functional identification and analysis of post-transcriptional regulators in vivo through the integration of molecular, cellular and experimental biology, transgenic systems and functional genomics.

The lab is also supervising Flow Cytometry Unit and Transgenesis Unit.