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doi: 10.2337/dc14-1596

Since enhanced HIF1a signaling in the hippocampus has been shown to contribute to the pro-oxidant condition caused by IH 22 and Tbr2 + INPs are susceptible to oxidative stress 34 , we next examined how IH affected HIF1a expression among early neural precursors and the potential role that an IH-dependent pro-oxidant state has on Tbr2 + cells