ArticleMolecular and cellular biology1998
DDB, a putative DNA repair protein, can function as a transcriptional partner of E2F1.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.
- Functional variants in DCAF4 associated with lung cancer risk in European populations.Carcinogenesis · 2017Pooled it
- DCAF4, a novel gene associated with leucocyte telomere length.Journal of medical genetics · 2015Pooled it
- Hepatocyte-specific loss of DDB1 attenuates hepatic steatosis but aggravates liver inflammation and fibrosis in MASH.Hepatology communications · 2024Article
- DDB2 represses epithelial-to-mesenchymal transition and sensitizes pancreatic ductal adenocarcinoma cells to chemotherapy.Frontiers in oncology · 2022Article
- The E2F1 transcription factor and RB tumor suppressor moonlight as DNA repair factors.Cell cycle (Georgetown, Tex.) · 2020Review
- DDB1 Stimulates Viral Transcription of Hepatitis B Virus via HBx-Independent Mechanisms.Journal of virology · 2016Article
- A DDB2 mutant protein unable to interact with PCNA promotes cell cycle progression of human transformed embryonic kidney cells.Cell cycle (Georgetown, Tex.) · 2015Article
- DNA repair initiation induces expression of ribonucleotide reductase in human chronic lymphocytic leukemia cells.Leukemia & lymphoma · 2014Article
- DNA damage-binding complex recruits HDAC1 to repress Bcl-2 transcription in human ovarian cancer cells.Molecular cancer research : MCR · 2014Article
- The deubiquitinating protein USP24 interacts with DDB2 and regulates DDB2 stability.Cell cycle (Georgetown, Tex.) · 2012Article
- E2F1 and p53 transcription factors as accessory factors for nucleotide excision repair.International journal of molecular sciences · 2012Review
- Damaged DNA binding protein 2 in reactive oxygen species (ROS) regulation and premature senescence.International journal of molecular sciences · 2012Review
- E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.PLoS pathogens · 2012Article
- Overexpression of DDB2 enhances the sensitivity of human ovarian cancer cells to cisplatin by augmenting cellular apoptosis.International journal of cancer · 2010Article
- E2F1 localizes to sites of UV-induced DNA damage to enhance nucleotide excision repair.The Journal of biological chemistry · 2010Article
- The role of the retinoblastoma/E2F1 tumor suppressor pathway in the lesion recognition step of nucleotide excision repair.DNA repair · 2009Article
- Identification of DDB2 protein as a transcriptional regulator of constitutive SOD2 gene expression in human breast cancer cells.The Journal of biological chemistry · 2009Article
- Human immunodeficiency virus type 1 Vif induces cell cycle delay via recruitment of the same E3 ubiquitin ligase complex that targets APOBEC3 proteins for degradation.Journal of virology · 2008Article
- Article
- Other proteins interacting with XP proteins.Advances in experimental medicine and biology · 2008Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor E2F1 is believed to be involved in the regulated expression of the DNA replication genes. To gain insights into the transcriptional activation function of E2F1, we looked for proteins in HeLa nuclear extracts that bind to the activation domain of E2F1. Here we show that DDB, a putative DNA repair protein, associates with the activation domain of E2F1. DDB was identified as a heterodimeric protein (48 and 127 kDa) that binds to UV-damaged DNA. We show that the UV-damaged-DNA binding activity from HeLa nuclear extracts can associate with the activation domain of E2F1. Moreover, the 48-kDa subunit of DDB, synthesized in vitro, binds to a fusion protein of E2F1 depending on the C-terminal activation domain. The interaction between DDB and E2F1 can also be detected by coimmunoprecipitation experiments. Immunoprecipitation of an epitope-tagged DDB from cell extracts resulted in the coprecipitation of E2F1. In a reciprocal experiment, immunoprecipitates of E2F1 were found to contain DDB. Fractionation of HeLa nuclear extracts also revealed a significant overlap in the elution profiles of E2F1 and DDB. For instance, DDB, which does not bind to the E2F sites, was enriched in the high-salt fractions containing E2F1 during chromatography through an E2F-specific DNA affinity column. We also observed evidence for a functional interaction between DDB and E2F1 in living cells. For instance, expression of DDB specifically stimulated E2F1-activated transcription. In addition, the transcriptional activation function of a heterologous transcription factor containing the activation domain of E2F1 was stimulated by coexpression of DDB. Moreover, DDB expression could overcome the retinoblastoma protein (Rb)-mediated inhibition of E2F1-activated transcription. The results suggest that this damaged-DNA binding protein can function as a transcriptional partner of E2F1. We speculate that the damaged-DNA binding function of DDB, besides repair, might serve as a negative regulator of E2F1-activated transcription, as damaged DNA will sequester DDB and make it unavailable for E2F1. Furthermore, the binding of DDB to damaged DNA might be involved in downregulating the replication genes during growth arrest induced by damaged DNA.
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