ArticleMolecular and cellular biology2008
The xeroderma pigmentosum group E gene product DDB2 activates nucleotide excision repair by regulating the level of p21Waf1/Cip1.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Analysis of Radiation Toxicity in Mammalian Cells Stably Transduced with MitochondrialInternational journal of molecular sciences · 2023Article
- Revisiting the Function of p21International journal of molecular sciences · 2022Review
- EZH2 has a non-catalytic and PRC2-independent role in stabilizing DDB2 to promote nucleotide excision repair.Oncogene · 2020Article
- Interplay between BRCA1 and GADD45A and Its Potential for Nucleotide Excision Repair in Breast Cancer Pathogenesis.International journal of molecular sciences · 2020Review
- The Role of the Cyclin Dependent Kinase Inhibitor p21Cancers · 2019Review
- Phosphorylated HBO1 at UV irradiated sites is essential for nucleotide excision repair.Nature communications · 2017Article
- UV Damage-Induced Phosphorylation of HBO1 Triggers CRL4DDB2-Mediated Degradation To Regulate Cell Proliferation.Molecular and cellular biology · 2016Article
- Histone H2AX Is Involved in FoxO3a-Mediated Transcriptional Responses to Ionizing Radiation to Maintain Genome Stability.International journal of molecular sciences · 2015Article
- Orchestral maneuvers at the damaged sites in nucleotide excision repair.Cellular and molecular life sciences : CMLS · 2015Review
- 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 damage-binding complex recruits HDAC1 to repress Bcl-2 transcription in human ovarian cancer cells.Molecular cancer research : MCR · 2014Article
- DDB2 association with PCNA is required for its degradation after UV-induced DNA damage.Cell cycle (Georgetown, Tex.) · 2014Article
- DDB2 suppresses epithelial-to-mesenchymal transition in colon cancer.Cancer research · 2013Article
- FOXP3 regulates sensitivity of cancer cells to irradiation by transcriptional repression of BRCA1.Cancer research · 2013Article
- Tumor regression by phenethyl isothiocyanate involves DDB2.Cancer biology & therapy · 2013Article
- The yin-yang of DNA damage response: roles in tumorigenesis and cellular senescence.International journal of molecular sciences · 2013Article
- Xeroderma pigmentosum: man deprived of his right to light.TheScientificWorldJournal · 2013Review
- The deubiquitinating protein USP24 interacts with DDB2 and regulates DDB2 stability.Cell cycle (Georgetown, Tex.) · 2012Article
- p21 cooperates with DDB2 protein in suppression of ultraviolet ray-induced skin malignancies.The Journal of biological chemistry · 2012Article
- Damaged DNA binding protein 2 in reactive oxygen species (ROS) regulation and premature senescence.International journal of molecular sciences · 2012Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The xeroderma pigmentosum group E gene product DDB2, a protein involved in nucleotide excision repair (NER), associates with the E3 ubiquitin ligase complex Cul4A-DDB1. But the precise role of these interactions in the NER activity of DDB2 is unclear. Several models, including DDB2-mediated ubiquitination of histones in UV-irradiated cells, have been proposed. But those models lack clear genetic evidence. Here we show that DDB2 participates in NER by regulating the cellular levels of p21(Waf1/Cip1). We show that DDB2 enhances nuclear accumulation of DDB1, which binds to a modified form of p53 containing phosphorylation at Ser18 (p53(S18P)) and targets it for degradation in low-dose-UV-irradiated cells. DDB2(-/-) mouse embryonic fibroblasts (MEFs), unlike wild-type MEFs, are deficient in the proteolysis of p53(S18P). Accumulation of p53(S18P) in DDB2(-/-) MEFs causes higher expression p21(Waf1/Cip1). We show that the increased expression of p21(Waf1/Cip1) is the cause NER deficiency in DDB2(-/-) cells because deletion or knockdown of p21(Waf1/Cip1) reverses their NER-deficient phenotype. p21(Waf1/Cip1) was shown to bind PCNA, which is required for both DNA replication and NER. Moreover, an increased level of p21(Waf1/Cip1) was shown to inhibit NER both in vitro and in vivo. Our results provide genetic evidence linking the regulation of p21(Waf1/Cip1) to the NER activity of DDB2.
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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.