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Current Projects

Targeting Phosphatase Regulated Cleavage of HIF-1α in Ischemic Brain Injury (R01 / NINDS)

De novo gene expression regulated by the hypoxia inducible factor-1α (HIF-1α) plays a decisive role in determining whether neurons live or die after an ischemic insult. While the molecular mechanisms regulating the balance between HIF’s adaptive and pathological effects remain unsettled, evidence supports a role for changes in HIF-1α dependent post-translational modifications (PTMs). Utilizing a combination of in vitro and in vivo modeling, this project seeks to understand how physiologically responsive PTMs and site-specific cleavage of HIF-1α influences neuron survival in the post-ischemic brain.

Defining Neurotherapeutic Targets in Hypoxia-Induced CHOP-10 Signaling Networks (R00 / NINDS)

The endoplasmic reticulum plays a central role in the cellular response to ischemia. However, the mechanisms governing the balance between ER-dependent protective and damaging responses remain unsettled. We have shown that the bZIP factor CHOP-10, previously linked to ER stress, differentiation and apoptosis, is both BDNF-responsive and neuroprotective in certain contexts. These observations suggest that CHOP-10 plays a more complex role after injury than previously recognized. In addition to defining the network of ER-responsive sensor-effector loops involved in regulating neuron survival after ischemic insult, we are also investigating how BDNF-CHOP-10 coupling regulates the fate and development of cells in the central nervous system.