Pin1 levels are downregulated during ER stress in human neuroblastoma cells.

Previously, we showed that pretangle neurons in Alzheimer's disease (AD) brain display unfolded protein stress in the endoplasmic reticulum (ER). Others showed that the peptidylprolyl isomerase Pin1 protects against tangle formation by facilitating tau dephosphorylation, corroborating with the lower expression of Pin1 observed in tangle-bearing neurons. In this study, we investigated Pin1 expression under ER stress conditions. We show that in human, but not mouse neuroblastoma cells, Pin1 is downregulated in response to ER stress, in accordance with the presence of an ER stress response element in the mouse, but not the human Pin1 gene. This study creates a starting point to investigate whether modulation of the ER stress response may prevent or delay tau pathology in AD.