Post-Comprehensive Research Awards

• Katherine Perschbacher (MCB Graduate Student, Grobe lab) - Preeclampsia is a serious cardiovascular condition characterized by late gestational onset of hypertension and can lead to multisystem organ failure and death. Our lab has demonstrated a significant relationship between elevated plasma levels of vasopressin (AVP) during the first six weeks of gestation in women who later developed preeclampsia. AVP activates signaling cascades through V1A and V2 receptors, which signal through Gαq11 and Gαs second messenger systems. RGS proteins in the RGS-B/R4 family act as endogenous brakes on G-protein signaling cascades by accelerating GTP hydrolysis of Gαq/11 subunits to stop second messenger activation. We are investigating the potential role of RGS-B/R4 proteins in the predisposition of women to preeclampsia.
• Addison Woll (MCB Graduate Student, Sigmund lab) - Hypertension is the leading preventable risk factor for a variety of diseases including kidney failure, heart failure, and death. Our lab has shown the role of Peroxisome Proliferator-Activated Receptor gamma (PPARg) in regulating blood pressure in the vascular system. Retinol Binding Protein 7 (RBP7) was identified in the lab as a novel PPARg target gene, only appreciably expressed in the vascular endothelium. It was further discovered that a global knockout of RBP7 resulted in the failure of PPARg to rescue endothelial dysfunction in mice. Since the endothelium plays an important role in regulation of blood pressure, my project is to determine the mechanism behind the interaction of PPARg and RBP7 in the endothelium.
• Jennie Liu (Graduate Student, Strack lab) - Mitochondria are dynamic organelles that form a network which constantly undergoes fusion and fission, both are important for our body to stay functional and healthy. New data have shown that mitochondria in neurons after stroke are very fragmented, one of my research projects is aimed at further characterizing the underlying molecular mechanisms of this fascinating observation in order to find a new drug target for stroke. Unlike stroke where mitochondria fission is considered undesirable, Autosomal Recessive Spatic Ataxia of Charlevoix-Saguenay (ARSACS) displays the exact opposite mitochondria phenotype. Our lab developed a technique where we can chemically induce mitochondria fission by using a FDA approved drug named rapamycin. Currently, we have already tested this technique in cultured neurons.
• Jianing Song (Graduate Student, Strack lab) - Single genetic mutations are largely accounted for X-linked intellectual disability (XLID). My dissertation research is to study the structural and functional differences of the XLID-causing mutations in KLHL15 (Kelch-like protein 15), which is a key component of the protein degradation system (E3 ubiquitin ligase), and elucidate the molecular mechanism(s) underlying KLHL15-associated XLID pathogenicity.

Ballard Seashore Dissertation Fellowship

• Kyle Flippo (Graduate Student, Strack lab) - Stroke is the 5th leading cause of death in the United States with no preventative therapies available.  Compelling evidence suggests that mitochondria, a sub-cellular organelle important for cellular energy production, may provide a new therapeutic target. Inhibiting fission of mitochondria prevents brain damage during stroke however, the mechanism is poorly understood. Using in vivo mouse models we find that inhibiting mitochondrial fission improves mitochondrial bioenergetics preventing brain damage while promoting fission has the opposite effect.