ArticleMolecular & cellular proteomics : MCP2010
Differential proteomics analysis reveals a role for E2F2 in the regulation of the Ahr pathway in T lymphocytes.
Article in Molecular & cellular proteomics : MCP, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 27 citations in OpenAlex.
- Expression patterns of E2Fs identify tumor microenvironment features in human gastric cancer.PeerJ · 2024Article
- Article
- E2F1/2/4 mRNA is associated with immune infiltration and are potential biomarkers for the prognosis of human gastric carcinoma.Translational cancer research · 2021Article
- Article
- Meta-Analysis of Transcriptome Data Detected New Potential Players in Response to Dioxin Exposure in Humans.International journal of molecular sciences · 2020Article
- Multigenerational and Transgenerational Effects of Dioxins.International journal of molecular sciences · 2019Review
- Deacetylation of NAT10 by Sirt1 promotes the transition from rRNA biogenesis to autophagy upon energy stress.Nucleic acids research · 2018Article
- The nuclear protein ALY binds to and modulates the activity of transcription factor E2F2.Molecular & cellular proteomics : MCP · 2013Article
- Identification of co-occurring transcription factor binding sites from DNA sequence using clustered position weight matrices.Nucleic acids research · 2012Article
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
E2F transcription factors (E2F1-8) are best known for their role in cell proliferation, although it is clear that they regulate many other biological processes through the transcriptional modulation of distinct target genes. However, the specific set of genes regulated by each E2F remains to be characterized. To gain insight into the molecular pathways regulated by E2F2, we have analyzed the proteome of antigen receptor-activated T cells lacking E2F2. We report that loss of E2F2 results in a deregulated Aryl-hydrocarbon-receptor pathway. Proliferating E2F2(-/-) T lymphocytes expressed significantly higher levels of Aip, Ahr, and Arnt relative to wild-type (WT)(1) controls. The mechanism for increased levels of Aip appears straightforward, involving direct regulation of the Aip gene promoter by E2F2. Although the Ahr and Arnt promoters also bind E2F2, their regulation appears to be more complex. Nevertheless, exposure to the environmental xenobiotic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a well-known exogenous ligand of the Ahr pathway, led to overexpression of the Ahr target gene Cyp1a1, and to increased sensitivity to TCDD-triggered apoptosis in E2F2(-/-) T cells compared with WT controls. These results suggest that E2F2 modulates cellular sensitivity to xenobiotic signals through the negative regulation of the Ahr pathway.
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