ArticleDevelopment (Cambridge, England)2014
TRIP/NOPO E3 ubiquitin ligase promotes ubiquitylation of DNA polymerase η.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- CDK-driven phosphorylation of TRAIP is essential for mitotic replisome disassembly and MiDAS.Nucleic acids research · 2025Article
- TRAIP resolves DNA replication-transcription conflicts during the S-phase of unperturbed cells.Nature communications · 2023Article
- ZNF212 promotes genomic integrity through direct interaction with TRAIP.Nucleic acids research · 2023Article
- Translesion DNA synthesis-driven mutagenesis in very early embryogenesis of fast cleaving embryos.Nucleic acids research · 2022Article
- Article
- CUL2EMBO reports · 2021Article
- Mechanisms of eukaryotic replisome disassembly.Biochemical Society transactions · 2020Review
- Molecular cloning, expression, overproduction and characterization of human TRAIP Leucine zipper protein.Saudi journal of biological sciences · 2020Article
- Mitotic replisome disassembly depends on TRAIP ubiquitin ligase activity.Life science alliance · 2019Article
- Nucleolar residence of the seckel syndrome protein TRAIP is coupled to ribosomal DNA transcription.Nucleic acids research · 2018Article
- Review
- Review
- Regulation of Mammalian DNA Replication via the Ubiquitin-Proteasome System.Advances in experimental medicine and biology · 2017Review
- TRAIP is a PCNA-binding ubiquitin ligase that protects genome stability after replication stress.The Journal of cell biology · 2016Article
- TRAIP promotes DNA damage response during genome replication and is mutated in primordial dwarfism.Nature genetics · 2016Article
- Functions of Ubiquitin and SUMO in DNA Replication and Replication Stress.Frontiers in genetics · 2016Review
- TRAIP regulates replication fork recovery and progression via PCNA.Cell discovery · 2016Article
- The TRAF-interacting protein (TRAIP) is a novel E2F target with peak expression in mitosis.Oncotarget · 2015Article
- Regulation of translesion DNA synthesis: Posttranslational modification of lysine residues in key proteins.DNA repair · 2015Review
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
We previously identified a Drosophila maternal effect-lethal mutant named 'no poles' (nopo). Embryos from nopo females undergo mitotic arrest with barrel-shaped, acentrosomal spindles during the rapid cycles of syncytial embryogenesis because of activation of a Chk2-mediated DNA checkpoint. NOPO is the Drosophila homolog of human TNF receptor associated factor (TRAF)-interacting protein (TRIP), which has been implicated in TNF signaling. NOPO and TRIP contain RING domains closely resembling those of known E3 ubiquitin ligases. We herein sought to elucidate the mechanism by which TRIP/NOPO promotes genomic stability by performing a yeast two-hybrid screen to identify potential substrates/interactors. We identified members of the Y-family of DNA polymerases that facilitate replicative bypass of damaged DNA (translesion synthesis) as TRIP interactors. We show that TRIP and NOPO co-immunoprecipitate with human and Drosophila Polη, respectively, from cultured cells. We generated a null mutation in Drosophila Polη (dPolη) and found that dPolη-derived embryos have increased sensitivity to ultraviolet irradiation and exhibit nopo-like mitotic spindle defects. dPolη and nopo interact genetically in that overexpression of dPolη in hypomorphic nopo-derived embryos suppresses nopo phenotypes. We observed enhanced ubiquitylation of Polη by TRIP and NOPO E3 ligases in human cells and Drosophila embryos, respectively, and show that TRIP promotes hPolη localization to nuclear foci in human cells. We present a model in which TRIP/NOPO ubiquitylates Polη to positively regulate its activity in translesion synthesis.
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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.