ArticleGenes & genomics2019
Hip2 ubiquitin-conjugating enzyme has a role in UV-induced G1/S arrest and re-entry.
Article in Genes & genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
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- Proteomics identifies apoptotic markers as predictors of histological transformation in patients with follicular lymphoma.Blood advances · 2023Article
- From seeds to trees: how E2 enzymes grow ubiquitin chains.Biochemical Society transactions · 2023Review
- The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy.International journal of molecular sciences · 2021Review
- The UBA domain of conjugating enzyme Ubc1/Ube2K facilitates assembly of K48/K63-branched ubiquitin chains.The EMBO journal · 2021Article
- ALS-Related Mutant SOD1 Aggregates Interfere with Mitophagy by Sequestering the Autophagy Receptor Optineurin.International journal of molecular sciences · 2020Article
- The immunostimulatory effect of indole-6-carboxaldehyde isolated fromAnimal cells and systems · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulation of cell cycle arrest and re-entry triggered by DNA damage is vital for cell division and growth and is also involved in cell survival. UV radiation can generate lesions in the DNA, which results in cell cycle arrest and the induction of the DNA repair process. However, the mechanism of promoting cell cycle progression following DNA repair is elusive. The primary aim of this study is to investigate whether Hip2 ubiquitin-conjugating enzyme has a role in UV-induced G1/S arrest and re-entry. The phase of HEK293 cells was synchronized at the G1/S border using thymidine. The synchronously proliferating cells were exposed to UV radiation to cause DNA damage. We investigated the expression of p53, Hip2, p21, cyclin D and E proteins that are involved in the cell cycle progression. Finally, we examined changes in the phosphorylation of Hip2 after UV radiation treatment using the pIMAGO™ assay. When cells were exposed to UV radiation, expression of p53 was elevated, and the cell cycle was arrested at the G1/S boundary. In response to the increased p53 level, Hip2 became phosphorylated and activated through the inhibition of its degradation. The phosphorylated Hip2 inhibited p53, thereby suppressing the expression of p21, a downstream signal, and sequentially stimulating cyclin D and cyclin E to induce re-entry to the cell cycle. Our studies demonstrate that Hip2 works as a regulator in UV-induced cell cycle arrest and re-entry.
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