Research Interests:
The actin cytoskeleton forms the framework that underlies cell morphology and motility. My research aims to understand how a cell's shape, its physiology and its motility are affected by signals and injuries that change the organization of actin. A major focus is the role of rho family GTPase signaling and regulation of actin binding proteins.
Two main areas of interest are currently represented in the laboratory:
- Ischemic acute renal failure is characterized by reversible injury to proximal tubule epithelial cells. An early manifestation of injury is disruption of normal cytoskeletal organization that in turn results in loss of normal cell polarity with consequent physiological abnormalities. We have shown that rho GTPase signaling is disrupted in an in vitro model of renal ischemia, and are currently investigating effector pathways downstream of rho that are affected by injury, and upstream pathways that lead to altered rho GTPase activity.
- We aim to understand how rho GTPases transduce signals to cause appropriate changes in cell morphology and motility in hematopoietic cells by using mice deficient in rho GTPases. We are investigating how defective rho GTPase signaling affects actin binding protein regulation using this unique in vivo system, and the effects of specific defects on inflammatory mediators of ischemia-reperfusion injury in the kidney.
Specific techniques employed include 2-photon and confocal fluorescence imaging of live cells and tissues, cell culture and transfection, protein isolation and transgenic and knockout animals.
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