Signal integration in the endoplasmic reticulum unfolded protein response

By D. Ron, Peter Walter. Nature reviews. Molecular cell biology, 2007

6,391 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/f96c5f702db9e26ccfd53eb5d549f5f86a7c3a3e

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Citations in the corpus

Measuring ER stress and the unfolded protein response using mammalian tissue culture system (2011, background): “Recent evidence further indicates that ER stressmediated cell dysfunction and death is involved in the pathogenesis of human chronic disorders, including diabetes and neurodegeneration (Ron and Walter, 2007).”
Treatment of Obesity with Celastrol (2015, neutral): “Perturbations of endoplasmic reticulum (ER) homeostasis, predominantly triggered by the accumulation of unfolded proteins, lead to the development of a condition referred to as ER stress (Lee and Ozcan, 2014; Park and Ozcan, 2013; Ron and Walter, 2007) and activate a complex signaling cascade called”
Toll-like receptor activation of XBP1 regulates innate immune responses in macrophages (2010, background): “org/molecule/query?afcsid=A003134">A003134 ) and PERK) and a transcription factor precursor (ATF6) that instigate distinct signaling pathway”
Reactive Oxygen Species in Health and Disease (2012, background): “However, if the stress is extreme or prolonged, cellular homeostasis cannot be established and, alternatively, cellular pathways culminating in apoptosis will be activated [33, 34].”
Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “Once activated, these three effectors decrease protein translation and promote expression of foldases and chaperones or proteins involved in the degradation of misfolded proteins [63,64].”
Pathophysiology of placental‐derived fetal growth restriction (2018, background): “pathways collectively known as the unfolded protein response (UPR).(71,72)”
Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Multiple disturbances can cause accumulation of unfolded proteins in the ER, triggering an evolutionarily conserved response termed the unfolded protein response (UPR”
Proteotoxic stress and inducible chaperone networks in neurodegenerative disease and aging. (2008, background): “Chaperones are abundantly expressed in multiple compartments of the cell and are thought to comprise a significant fraction of the cellular machinery (Bukau et al. 2006; Ron and Walter 2007).”
Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging (2009, methodology): “2] (57), anti-myosin heavy chain A [5-6] (57) or anti-dynamin-1 antibodies (29).”
Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, neutral): “The PERK arm of the UPR serves to halt protein translation, essentially by inactivating eukaryotic translation initiation factor 2 a (Ron and Walter, 2007).”
With TOR less is more: a key role for the conserved nutrient sensing TOR pathway in aging (2010, neutral): “ER stress is caused by a mismatch between the load of unfolded/ misfolded proteins within the ER and the capacity of the cellular machinery to cope with it (Ron and Walter, 2007).”
Systems biology approach predicts immunogenicity of the yellow fever vaccine in humans (2008, methodology): “First, we studied the protein cytokine response in the blood of vaccinees at days 0, 1, 3, 7 and 21 after vaccination, using a 24-plex Luminex assay.”