The unfolded protein response: controlling cell fate decisions under ER stress and beyond

By C. Hetz. Nature reviews. Molecular cell biology, 2012

3,844 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/5204c95aa1e87cd4f8e91504b91fc16336c76b88

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Citations in the corpus

Decoding cell death signals in liver inflammation. (2013, background): “Conversely, accumulating unfolded proteins competitively displace GRP78 from IRE1a, ATF6 and PERK, leading to their activation and eventually to the upregulation of mechanisms that attempt to re-establish homeostasis, mainly involving (i) a general (but not complete) translational arrest, (ii) the u”
Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer (2017, positive): “BAX, BAK, PP2A, and GADD34 additionally modulate UPR signal strength, though how these factors influence cell fate under chronic ER stress in the TME is unknown (Hetz, 2012).”
Impairment of ceramide synthesis causes a novel progressive myoclonus epilepsy (2014, background): “If stress is extreme or sustained, this signaling pathway may activate prodeath processes such as apoptosis.(14) ER stress is induced either when unfolded proteins accumulate in the ER due to increased protein synthesis or defective protein secretion or when ER dysfunctions, induced by unbalances of”
Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease (2014, background): “In addition, the kinase domain of IRE1a also integrates ER stress with pro-inflammatory responses through direct binding with adaptor protein tumor necrosis factor alpha (TNFa) receptorassociated factor 2 (TRAF2) and subsequent activation of the nuclear factor-kappaB (NF-jB) and c-Jun N-terminal kin”
Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases (2014, background): “Huntingtin and huntingtin-associated protein 1 influence neuronal calcium signaling mediated by inositol-(1,4,5) triphosphate receptor type 1.”
New developments in goblet cell mucus secretion and function (2015, positive): “Misfolded proteins trigger an unfolded protein response (UPR) that is in turn coupled to inflammation.(64) Single mutations in mouse Muc2 can cause endoplasmic reticulum accumulation that triggers a UPR response and increased levels of inflammatory cytokines.”
The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “ER-induced apoptosis occurs via three primary pathways, including the IRE1/ASK1/JNK pathway, the caspase-12 kinase pathway, and the C/EBP homologous protein (CHOP)/GADD153 pathway (11, 12).”