ArticleThe Journal of biological chemistry2008
C/EBP homology protein (CHOP) interacts with activating transcription factor 4 (ATF4) and negatively regulates the stress-dependent induction of the asparagine synthetase gene.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 179 citations in OpenAlex.
- Multifaceted roles of KCTD17 in cellular homeostasis and disease.BMB reports · 2026Review
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- ATF4 and CHOP coordinate endoplasmic reticulum stress-responsive gene programs through enhancer activation and chromatin looping.Nucleic acids research · 2026Article
- Unfolding Resilience: Molecular Integration of the Integrated Stress Response and Mitochondrial UPR in Skeletal Muscle Homeostasis.Muscles (Basel, Switzerland) · 2026Review
- ATF4: Orchestrating Cellular Stress Adaptation, Metabolism, and Immune Regulation in Health and Disease.International journal of molecular sciences · 2026Review
- Review
- Notoginsenoside R1 modulates the ATF4-CHOP-Bcl2 signaling pathway to alleviate mitochondrial stress damage and apoptosis in asthmatic airway epithelial cells.Frontiers in immunology · 2026Article
- Pre-established ATF4 occupancy and chromatin organization instruct selective transcription activation during integrated stress response.Nature communications · 2025Article
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Emerging roles for integrated stress response signaling in homeostasis.The FEBS journal · 2025Review
- Transcriptional regulation of solute carrier family 6 member 9 gene.Molecular biology reports · 2025Article
- Acute treadmill exercise induces mitochondrial unfolded protein response in skeletal muscle of male rats.Biochimica et biophysica acta. Bioenergetics · 2025Article
- Neurocellular Stress Response to Mojave Type A Rattlesnake Venom: Study of Molecular Mechanisms Using Human iPSC-Derived Neural Stem Cell Model.Biomolecules · 2025Article
- Mcl-1 is a Gatekeeper Molecule to Regulate the Crosstalk Between Ferroptotic Agent-Induced ER Stress and TRAIL-Induced Apoptosis.Journal of cellular biochemistry · 2025Article
- Taohong Siwu Decoction alleviates high salt-induced calcium overload and ferroptosis in vascular endothelial cells in hypertension by regulating ATF4.Frontiers in nutrition · 2025Article
- ISR Modulators in Neurological Diseases.Current neuropharmacology · 2025Review
- IGHMBP2 deletion suppresses translation and activates the integrated stress response.Life science alliance · 2024Article
- Ferroptosis in cancer: From molecular mechanisms to therapeutic strategies.Signal transduction and targeted therapy · 2024Review
- Precision formulation, a new concept to improve dietary amino acid absorption based on the study of cationic amino acid transporters.iScience · 2024Article
- Integrated Stress Response (ISR) Pathway: Unraveling Its Role in Cellular Senescence.International journal of molecular sciences · 2023Review
54 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
C/EBP homology protein (CHOP), a stress-induced transcription factor, is involved in transcriptional regulation, cell cycle, and apoptosis. The present studies identified CHOP as an interacting partner of activating transcription factor (ATF) 4 in a yeast two-hybrid screen and confirmed their interaction in HEK293T cells. CHOP protein levels rose modestly and transiently during amino acid deprivation, whereas endoplasmic reticulum stress caused a much higher and sustained expression of CHOP protein. Exogenous CHOP expression enhanced the TRB3 gene induction by amino acid deprivation. Conversely, CHOP suppressed the induction of the endogenous asparagine synthetase (ASNS) gene and inhibited transcription from a reporter gene driven by the ASNS promoter following activation by ATF4 or amino acid deprivation. Short interfering RNA-mediated knockdown of CHOP further enhanced the induction of ASNS by either amino acid deprivation or endoplasmic reticulum stress. The CHOP-dependent repression of the ASNS gene required the entire CHOP protein, arguing against the possibility of simple sequestration of ATF4 by the CHOP leucine zipper domain, and chromatin immunoprecipitation analysis showed association of CHOP with the ASNS and TRB3 promoters. Interestingly, chromatin immunoprecipitation also showed that CHOP was associated with the C/EBP-ATF composite site regions of the SNAT2, VEGF, and CAT-1 genes, despite no significant effect on their expression after exogenous CHOP overexpression. Collectively, the results document that CHOP is a member of the transcription factor network that controls the stress-induced regulation of specific C/EBP-ATF-containing genes, such as ASNS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.