Roles of CHOP/GADD153 in endoplasmic reticulum stress

By S. Oyadomari, Masataka Mori. Cell Death and Differentiation, 2004

2,891 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7a8e9a07984a0bb80ffcd93245f2f702d42e5450

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In Cell Biology

1. R. Kaufman
2. H. Chae
3. Hyung-Ryong Kim
4. Afshin Samali
5. John Calvin Reed
6. A. Gorman
7. D. Minckler
8. Inki Kim

In Epidemiology

1. T. Ueno
2. E. Kominami
3. I. Tanida
4. D. Minckler
5. H. Chae
6. Hyung-Ryong Kim
7. Afshin Samali
8. John Calvin Reed

In Molecular Biology

1. R. Kaufman
2. Afshin Samali
3. A. Gorman
4. H. Chae
5. Hyung-Ryong Kim
6. J. Avruch
7. Philippe Lambin
8. Sanjeev Gupta

Citations in the corpus

• The unfolded protein response protects human tumor cells during hypoxia through regulation of the autophagy genes MAP1LC3B and ATG5. (2010, background): “Here we show that ATG5 is a direct target of CHOP, which, besides autophagy (as shown here), has also been shown to regulate apoptosis (73, 74).”
• The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “damage by alkylating agents (131, 133); it is thus not a specific”
• Chronic palmitate but not oleate exposure induces endoplasmic reticulum stress, which may contribute to INS-1 pancreatic beta-cell apoptosis. (2006, background): “Furthermore, palmitate, but not oleate, up-regulated the levels of the CHOP transcription factor, which in part mediates ER stress-induced cell death (35).”
• 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).”
• ER stress (PERK/eIF2α phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation (2007, background): “region, called ‘uORF bypath scanning system’.(35,36) ATF4 upregulates the transcription of downstream genes, including CHOP.”
• Glaucoma (2018, positive): “Microbeads made of latex and ferromagnetic polystyrene have also been utilized in primates, rats, and mice [8, 15, 17, 18].”
• Initiation and execution of lipotoxic ER stress in pancreatic β-cells (2008, background): “The PERK pathway induces apoptosis via ATF4 overexpression and consequent CHOP (Oyadomari and Mori, 2004; Zinszner et al., 1998) and ATF3 (Jiang et al., 2004; Ma et al., 2002) induction.”
• Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “A) CHOP/GADD153.”
• ER stress: Autophagy induction, inhibition and selection (2015, background): “ER stress can stimulate at least 3 apoptotic signals, including both intrinsic and extrinsic pathways.(27) The first and most vital mechanism of ER stress-induced apoptosis is mediated through DDIT3, which regulates cell death through diverse mechanisms.”
• Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “CHOP is a member of the C/EBP family of bZIP transcription factors that is induced by ER stress (reviewed in Ref”
• ER stress-induced cell death mechanisms. (2013, background): “CHOP/ GADD153 (growth arrest/DNA damage) plays a convergent role in the UPR and it has been identified as one of the most important mediators of ER stress-induced apoptosis protein (reviewed by [16]).”
• The Role of the PERK/eIF2α/ATF4/CHOP Signaling Pathway in Tumor Progression During Endoplasmic Reticulum Stress (2016, background): “On the other hand, under prolonged ER stress conditions, ATF4 promotes expression of transcription factors such as C/EBP homologous protein (CHOP), also termed growth arrest and DNA damage inducible gene (GADD135) [103, 104].”
• Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes (2007, background): “As with BAX, however, increased production of DDIT3 is not always sufficient to trigger cell death, although upregulation is indicative of an enhanced apoptotic potential [47, 48].”