ER stress (PERK/eIF2α phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation
By Y. Kouroku, E. Fujita, I. Tanida, T. Ueno, A. Isoai, H. Kumagai, S. Ogawa, R. Kaufman, E. Kominami, T. Momoi. Cell Death and Differentiation, 2007
988 citations recorded by the source corpus.
Subfields: Cell Biology, Cellular and Molecular Neuroscience, Epidemiology
View Paper: https://www.semanticscholar.org/paper/bb669933eb10e8f42bb2412f2654d78714c4f213
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In Cell Biology
- D. Klionsky
- I. Slaninová
- N. Mizushima
- Beth Levine
- Guido Kroemer
- G. Hotamışlıgil
- V. Deretic
- Alec C. Kimmelman
In Cellular and Molecular Neuroscience
- N. Mizushima
- D. Rubinsztein
- Beth Levine
- M. Jäättelä
- M. Høyer-Hansen
- Fiona M Menzies
- D. Klionsky
- Sovan Sarkar
In Epidemiology
- Beth Levine
- D. Klionsky
- N. Mizushima
- Guido Kroemer
- I. Slaninová
- V. Deretic
- Alec C. Kimmelman
- D. Rubinsztein
Citations in the corpus
- Guidelines for the use and interpretation of assays for monitoring autophagy (2012, background): “In this regard, the transcriptional induction of LC3 may be necessary to replenish the LC3 protein that is turned over during extensive ER stress- and hypoxia-induced autophagy.(443,448) Thus, assessing the mRNA levels of LC3 and other autophagy-related genes by northern blot or qRT-PCR may provide ”
- Autophagy and the integrated stress response (2010, positive): “Cells that carry a nonphosphorylatable mutant of eIF2a (S51A) fail to induce autophagy in response to starvation, suggesting that eIF2a phosphorylation on serine 51 (and by extension eIF2a kinases) plays a major role in autophagy regulation (Kouroku et al., 2007; Talloczy et al., 2002).”
- Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance (2010, background): “…of autophagic vesicles (Axe et al., 2008; Razi et al., 2009) and that experimental ER stress can induce autophagy in mammalian cells (Ogata et al., 2006), with several canonical UPR (unfolded protein response) pathways implicated in this interaction (Kouroku et al., 2007; Ogata et al., 2006).”
- Protein quality control in the early secretory pathway (2008, background): “On the one hand, blocking ERAD stimulates autophagy via signalling pathways that involve elements of the UPR- and Ire1-dependent JNK phosphorylation (Yorimitsu et al, 2006; Hosokawa et al, 2007; Kouroku et al, 2007; Yorimitsu and Klionsky, 2007).”
- Caspase 3-mediated stimulation of tumor cell repopulation during cancer radiotherapy (2011, neutral): “-iPLA2 (1-751) 4T 1 4T 1+ 4T 1- 4T 1-s -Full-length iPLA2(1-751) -cleaved iPLA2(453-751) B -iPLA2(453-751) -β actin A --actin”
- Autophagy and chemotherapy resistance: a promising therapeutic target for cancer treatment (2013, background): “PERK/eIF2a phosphorylation has been shown to be essential for the transcription of key autophagy-associated genes during ER stress and may mediate the polyglutamine-induced LC3 conversion.(19) The activation of IRE1/JNK promotes phosphorylation of Bcl-2 and p53, resulting in interfering with Bcl-2 b”
- ER stress: Autophagy induction, inhibition and selection (2015, background): “Evidence suggests that under ER stress conditions, the EIF2AK3 branch of the UPR helps to regulate those genes.103 The association of EIF2AK3 in ER stress-mediated autophagy was first documented by Kouroku et al.104 Specifically, they showed that aggregated polyglutamine (polyQ) proteins in the cyto”
- The integrated stress response (2016, positive): “In addition, PERK-mediated phosphorylation of eIF2a mediates increased ATG12 and LC3 conversion upon the expression of polyQ72 aggregates in C2C5 cells [98].”