ArticleMolecular immunology2009
CCAAT/enhancer binding proteins alpha and beta regulate the tumor necrosis factor receptor 1 gene promoter.
Article in Molecular immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
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- Tumor necrosis factor-α induces proliferation and reduces apoptosis of colorectal cancer cells through STAT3 activation.Immunogenetics · 2023Article
- Analysis of the Genetic Relationship between Atherosclerosis and Non-Alcoholic Fatty Liver Disease through Biological Interaction Networks.International journal of molecular sciences · 2023Article
- Single-Cell Transcriptomics-Based Study of Transcriptional Regulatory Features in the Non-Obstructive Azoospermia Testis.Frontiers in genetics · 2022Article
- EBNA2-deleted Epstein-Barr virus (EBV) isolate, P3HR1, causes Hodgkin-like lymphomas and diffuse large B cell lymphomas with type II and Wp-restricted latency types in humanized mice.PLoS pathogens · 2020Article
- B cells infected with Type 2 Epstein-Barr virus (EBV) have increased NFATc1/NFATc2 activity and enhanced lytic gene expression in comparison to Type 1 EBV infection.PLoS pathogens · 2020Article
- An EBNA3C-deleted Epstein-Barr virus (EBV) mutant causes B-cell lymphomas with delayed onset in a cord blood-humanized mouse model.PLoS pathogens · 2018Article
- Inflammatory factor TNF-α promotes the growth of breast cancer via the positive feedback loop of TNFR1/NF-κB (and/or p38)/p-STAT3/HBXIP/TNFR1.Oncotarget · 2017Article
- Glucocorticoid-induced microRNA-511 protects against TNF by down-regulating TNFR1.EMBO molecular medicine · 2015Article
- TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm weakness.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-α-PU.1 pathway.Nature medicine · 2011Article
- The Epstein-Barr virus BZLF1 protein inhibits tumor necrosis factor receptor 1 expression through effects on cellular C/EBP proteins.Journal of virology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
CCAAT/enhancer binding protein (C/EBP) transcription factors play essential roles in regulating an array of cellular processes, including differentiation, energy metabolism, and inflammation. In this report we demonstrate that both C/EBPalpha and C/EBPbeta activate the promoter driving transcription of the tumor necrosis factor receptor 1 (TNFR1). TNFR1 is the major receptor for tumor necrosis factor (TNF), a critical cytokine mediator of the inflammatory response. Although the TNFR1 protein has been shown to be regulated through post-translational modifications, very little is known about the transcriptional regulation of the TNFR1 gene. Here we have identified a specific C/EBP binding site within the TNFR1 promoter, and shown that this site is required for both C/EBPalpha and C/EBPbeta activation of the promoter in reporter gene assays. Furthermore, we show that both C/EBPalpha and C/EBPbeta are bound to the TNFR1 promoter in cells using chromatin immunoprecipitation assays. Finally, we demonstrate that reducing the level of C/EBPalpha and C/EBPbeta expression in cells using siRNA technology leads to decreased expression of the TNFR1 protein. These results suggest that the C/EBPalpha and C/EBPbeta transcription factors enhance expression of the TNFR1 protein in cells. Given that TNF and C/EBPbeta are known to activate each other's expression, C/EBPbeta may greatly amplify the initial TNF signal through a positive auto-regulatory mechanism.
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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.