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doi: 10.1016/j.carbpol.2017.10.049 186 TongAJHuRKWuLXLvXCLiXZhaoLNet al
However, prolonged activation of UPR leads to activation of JNK, glycogen synthase kinase 3 (GSK3), and transcription factor CCAAT/enhancer-binding homologous protein (CHOP), all of which upregulate pro-death proteins such as p53 up-regulation of apoptosis regulators (PUMA) and extrinsic pathways including tumor necrosis factor (TNF)-associated apoptosis-inducing ligands (TRAIL) to induce cell death through transcriptional upregulation of TRAIL receptor 2 (TRAIL-R2) expression
Crossing boundaries: Interplay between the immune system and oligodendrocyte lineage cells
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Significantly, neurons from mice expressing a CaMKK2 mutant that mimics constitutive GSK3 phosphorylation of the S3-node, have neurite outgrowth abnormalities and fail to establish appropriate axon-dendrite polarity [40]
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