UPR, autophagy and mitochondria crosstalk underlies the ER stress response
By Daniela Senft, Z. Ronai. TIBS -Trends in Biochemical Sciences. Regular ed, 2015
1,039 citations recorded by the source corpus.
Cellular stress, induced by external or internal cues, activates several well-orchestrated processes aimed at either restoring cellular homeostasis or committing to cell death. Those processes include the unfolded protein response (UPR), autophagy, hypoxia, and mitochondrial function, which are part of the global ER stress (ERS) response. When one of the ERS elements is impaired, as often occurs under pathological conditions, overall cellular homeostasis may be perturbed. Further, activation of the UPR could trigger changes in mitochondrial function or autophagy, which could modulate the UPR, exemplifying cross-talk processes. Among the numerous factors that control the magnitude or duration of these processes are ubiquitin ligases, which govern overall cellular stress outcomes. Here we summarize crosstalk among fundamental processes governing ERS responses.
Subfields: Cell Biology, Epidemiology, Geriatrics and Gerontology
View Paper: https://www.semanticscholar.org/paper/52a983434b3ae15f0792bd88ef81343e80f3c9ba
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
In Epidemiology
Citations in the corpus
- Autophagy during viral infection — a double-edged sword (2018, background): “Moreover, autophagy is part of host stress responses such as the unfolded protein response (UPR) 10 . Given that viral infection and replication cause cell stress, autophagy is a frequent by-product of infection.”
- New insights into the interplay between autophagy, gut microbiota and inflammatory responses in IBD (2019, background): “Autophagy, unfolded protein response and ER stress are interconnected at many levels [39].”