ArticleNucleic acids research2000
CHOP gene expression in response to endoplasmic-reticular stress requires NFY interaction with different domains of a conserved DNA-binding element.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 74 citations in OpenAlex.
- CHOP overexpression sensitizes human non-small cell lung cancer cells to cisplatin treatment by Bcl-2/JNK pathway.American journal of translational research · 2021Article
- Sledgehammer to Scalpel: Broad Challenges to the Heart and Other Tissues Yield Specific Cellular Responses via Transcriptional Regulation of the ER-Stress Master Regulator ATF6α.International journal of molecular sciences · 2020Review
- Fibroblast Growth Factor 22 Inhibits ER Stress-Induced Apoptosis and Improves Recovery of Spinal Cord Injury.Frontiers in pharmacology · 2020Article
- Autophagy controls neonatal myogenesis by regulating the GH-IGF1 system through a NFE2L2- and DDIT3-mediated mechanism.Autophagy · 2019Article
- The thiosemicarbazone MeCell death & disease · 2018Article
- A non-canonical pathway regulates ER stress signaling and blocks ER stress-induced apoptosis and heart failure.Nature communications · 2017Article
- Endoplasmic reticulum stress induces PRNP prion protein gene expression in breast cancer.Breast cancer research : BCR · 2013Article
- Increased endoplasmic reticulum stress response is involved in clopidogrel-induced apoptosis of gastric epithelial cells.PloS one · 2013Article
- Gene regulatory network of unfolded protein response genes in endoplasmic reticulum stress.Cell stress & chaperones · 2013Article
- Free fatty acid induces endoplasmic reticulum stress and apoptosis of β-cells by Ca2+/calpain-2 pathways.PloS one · 2013Article
- Cellular iron depletion and the mechanisms involved in the iron-dependent regulation of the growth arrest and DNA damage family of genes.The Journal of biological chemistry · 2011Article
- Is there a common upstream link for autophagic and apoptotic cell death in human high-grade gliomas?Neuro-oncology · 2011Article
- Hepatitis E virus ORF2 protein activates the pro-apoptotic gene CHOP and anti-apoptotic heat shock proteins.PloS one · 2011Article
- Semliki forest virus-induced endoplasmic reticulum stress accelerates apoptotic death of mammalian cells.Journal of virology · 2010Article
- Unfolded protein response suppresses CEBPA by induction of calreticulin in acute myeloid leukaemia.Journal of cellular and molecular medicine · 2010Article
- The human SPT20-containing SAGA complex plays a direct role in the regulation of endoplasmic reticulum stress-induced genes.Molecular and cellular biology · 2009Article
- Brefeldin A activates CHOP promoter at the AARE, ERSE and AP-1 elements.Molecular and cellular biochemistry · 2008Article
- Endoplasmic reticulum stress exacerbates ischemia-reperfusion-induced apoptosis through attenuation of Akt protein synthesis in human choriocarcinoma cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2007Article
- Activation profiles of HSPA5 during the glomerular mesangial cell stress response to chemical injury.Cell stress & chaperones · 2007Article
- Dynamic recruitment of transcription factors and epigenetic changes on the ER stress response gene promoters.Nucleic acids research · 2006Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor CHOP/GADD153 gene is induced by cellular stress and is involved in mediating apoptosis. We report the identification of a conserved region in the promoter of the CHOP gene responsible for its inducibility by endoplasmic reticulum (ER) stress. Deletion mutants of the human CHOP promoter identify a region comprising nucleotides -75 to -104 required for both constitutive and ER-stress-inducible expression. This region of the promoter, the ER-stress element (ERSE) is sufficient to confer both increased basal activity and ER-stress inducibility to an otherwise inactive heterologous promoter. The CHOP ERSE is a novel variant of the ERSE as it contains two different functional domains, and a GA- instead of GC-rich intervening sequence. The CCAAT-box domain occupied by the constitutive transcriptional activator nuclear factor Y (NFY) is required for constitutive activation whereas the variant GCACG 'inducible' domain uniquely mediates ER-stress inducibility. By UV-crosslinking analysis NFY makes contact not only with the constitutive activator CCAAT box but also with the inducible GCACG domain. Deletions and nucleotide substitutions in the CCAAT box as well as its replacement by an SP1 site failed to support ER inducibility. These findings support the notion that NFY is not only required for constitutive activation of CHOP gene transcription, but is also an active and essential element for the assembly of an ER-stress-inducible enhanceosome that activates CHOP gene expression in response to cellular stress.
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