CAMK2G and ischemia: Bing-Ren et al. have shown that isolated neocortex protein from rats after global cerebral ischemia (GCI, 15 min ischemia, followed by 30 min, 4 h, and 24 h reperfusion) exhibited increased CaMKII immunoreactivity and CaM binding that peaked at 30 min after reperfusion in the crude synaptosomal fraction of hippocampal CA1 and CA3/DG (dentate gyrus) regions but decreased in the microsomal and cytosolic fractions, suggesting a translocation of CaMKII to synaptosomes [61].