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Deletion of GPRASP2 causes impaired synaptic communications and modulates the surface availability of mGluR5 in mice [61]
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Consistent with our findings, studies with mouse aortic endothelial cells isolated from GPx1 −/− and wildtype mice reported that GPx1-deficiency promotes ROS production (both superoxide and hydrogen peroxide), enhances MAPK and NFκB activation, and upregulates VCAM1 expression in response to TNFα [85]
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