ArticleNucleic acids research2021
ID3 promotes homologous recombination via non-transcriptional and transcriptional mechanisms and its loss confers sensitivity to PARP inhibition.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition.International journal of cancer · 2026Article
- A prevalent disease-associated SNP in the humanNAR molecular medicine · 2026Article
- The Quartet of Core Oncogenic Drivers in Neuroendocrine Prostate Cancer: Multi-Omics Dataset Integration to Forge a Translational Link Between Biology and Precision Therapy.International journal of biological sciences · 2026Review
- Tumor-infiltrating myeloid cells; mechanisms, functional significance, and targeting in cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Nuclear receptors as novel regulators that modulate cancer radiosensitivity and normal tissue radiotoxicity.Molecular cancer · 2025Review
- In situ spatial transcriptomic analysis of human skeletal muscle using the Xenium platform.Cell and tissue research · 2025Article
- Pathophysiological Features of Remodeling in Vascular Diseases: Impact of Inhibitor of DNA-Binding/Differentiation-3 and Estrogenic Endocrine Disruptors.Medical sciences (Basel, Switzerland) · 2024Review
- ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune response.Nucleic acids research · 2024Article
- Vitamin a potentiates sheep myoblasts myogenic differentiation through BHLHE40-modulated ID3 expression.BMC genomics · 2024Article
- Molecular mechanism of PARP inhibitor resistance.Oncoscience · 2024Review
- Heterogeneity in the gene regulatory landscape of leiomyosarcoma.NAR cancer · 2023Article
- A positive feedback loop between ID3 and PPARγ via DNA damage repair regulates the efficacy of radiotherapy for rectal cancer.BMC cancer · 2023Article
- Two rare cancers of the exocrine pancreas: to treat or not to treat like ductal adenocarcinoma?Journal of cancer metastasis and treatment · 2023Article
- Genome-wide investigations on regulatory functions of RECQ1 helicase.Methods (San Diego, Calif.) · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibitor of DNA-binding 3 (ID3) is a transcriptional regulator that limits interaction of basic helix-loop-helix transcription factors with their target DNA sequences. We previously reported that ID3 loss is associated with mutational signatures linked to DNA repair defects. Here we demonstrate that ID3 exhibits a dual role to promote DNA double-strand break (DSB) repair, particularly homologous recombination (HR). ID3 interacts with the MRN complex and RECQL helicase to activate DSB repair and it facilitates RAD51 loading and downstream steps of HR. In addition, ID3 promotes the expression of HR genes in response to ionizing radiation by regulating both chromatin accessibility and activity of the transcription factor E2F1. Consistently, analyses of TCGA cancer patient data demonstrate that low ID3 expression is associated with impaired HR. The loss of ID3 leads to sensitivity of tumor cells to PARP inhibition, offering new therapeutic opportunities in ID3-deficient tumors.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.