Ca²⁺ signalling system initiated by endoplasmic reticulum stress stimulates PERK activation.

ABSTRACT: The accumulation of unfolded proteins within the Endoplasmic Reticulum (ER) activates a signal transduction pathway termed the unfolded protein response (UPR), which attempts to restore ER homoeostasis. If this cannot be done, UPR signalling ultimately induces apoptosis. Ca²⁺ depletion in the ER is a potent inducer of ER stress. Despite the ubiquity of Ca²⁺ as an intracellular messenger, the precise mechanism(s) by which Ca²⁺ release affects the UPR remains unknown. Tethering a genetically encoded Ca²⁺ indicator (GCamP6) to the ER membrane revealed novel Ca²⁺ signalling events initiated by Ca²⁺ microdomains in human astrocytes under ER stress, induced by tunicamycin (Tm), an N-glycosylation inhibitor, as well as in a cell mo

SUBMITTER: Feliziani C 

PROVIDER: S-EPMC9982837 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature