Current research in our laboratory is focused on three major areas:

1. Investigating the pathogenesis of mucopolysaccharidosis type VII (MPS VII), a genetic disorder caused by a deficiency of β-glucuronidase, one of the eleven lysosomal enzymes required for the stepwise degradation of glycosaminoglycans (GAGs). Widespread lysosomal accumulation of undegraded or partially degraded GAGs leads to cellular and multi-organ dysfunction, resulting in premature death in most cases. Although the genetic causes of MPS VII have been known for years, the pathways linking lysosomal storage to cellular damage or death remain unclear. We address these unresolved questions using a novel Drosophila model of the disease, developed in our laboratory. Currently, we are actively investigating the mechanisms of neurodegeneration and developmental defects associated with MPS VII.
2. Understanding how macrophage-dwelling Leishmania parasite utilize the lysosome as their replicative niche is a major focus of our research. Macrophages typically rely on the acidic and proteolytic environment of the lysosome to destroy engulfed pathogens. However, some pathogens like Leishmania have evolved strategies to survive and even replicate under these harsh conditions. Using a in vitro macrophage cell culture and in vivo mice model of Leishmania infection, we investigate: (a) how the pathogen acclimatize with and thrive in the acidic pH of the lysosome, and (b) how the intracellular pathogen compete with the host for acquisition of essential nutrients such as glucose and iron.
3. In collaboration with chemists, we are developing lysosomal targeting technologies aimed at effectively delivering antileishmanial drugs or the missing enzyme for MPS VII (β-glucuronidase) to the lysosomal compartment. Once established, we will evaluate the efficacy of these delivery systems in our animal models of the diseases. 

   The progress we have made in each of the above areas can be found in our publication list