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Thus, the accelerated resistance previously observed (Figure 1) does not appear to be due to an altered genotype

Interestingly, occludin knockout mice had morphologically intact tight junctions but displayed complex histological phenotypes, with chronic inflammation and a defective epithelial barrier, which implicated that its crucial role was in tight junction stability rather than tight junction assembly

Recent studies have revealed that calpain-2 conditional knockout mice are protected against the pathological consequences of repeated mild TBI and that genetic deletion or pharmaceutical inhibition of calpain-2 prevented alterations in the subcellular localization of TDP-43