ArticleCell death and differentiation2023
p53-dependent DNA repair during the DNA damage response requires actin nucleation by JMY.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Identification of MKRN1 as a key modulator of the p53-MDM2 feedback loop.Cell death and differentiation · 2026Article
- Plant Bioactive Constituents and Their Potential Benefits in HPV-Positive Oropharyngeal Squamous Cell Carcinoma-A Narrative Review.Current issues in molecular biology · 2026Review
- PHF20 stabilizes the GAS7-F-actin axis to drive DNA damage repair and chemoresistance in cutaneous squamous cell carcinoma.Cell death & disease · 2026Article
- Junction-mediating and regulatory protein (JMY) is a promoting protein for radial migration of cortical neurons.Cell death discovery · 2026Article
- Genotoxicity and gene expression modulation associated with the use of DDVP antiparasitic drugs in aquaculture onFrontiers in veterinary science · 2026Article
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- Synergistic Induction of Apoptosis by Boswellic Acid and Cisplatin in A549 Lung Cancer Cells Through NF-κB Modulation and p53 Pathway Activation.Current issues in molecular biology · 2025Article
- Deep Proteomics Analysis Unravels the Molecular Signatures of Tonsillar B Cells in PFAPA and OSAS in the Pediatric Population.International journal of molecular sciences · 2025Article
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- HNMT Promotes the Occurrence and Progression of Nasopharyngeal Carcinoma by Inhibiting the IFN/TXNIP/p53 Axis.Current medical science · 2025Article
- Review
- Impact of semaphorin, Sema3F, on the gene transcription and protein expression of CREB and its binding protein CREBBP in primary hippocampal neurons of rats.Open life sciences · 2025Article
- Unveiling the molecular profile of a prostate carcinoma: implications for personalized medicine.Biology direct · 2024Article
- Mice with NOP2/sun RNA methyltransferase 5 deficiency die before reaching puberty due to fatal kidney damage.Renal failure · 2024Article
- DNA Damage and Inflammatory Response of p53 Null H358 Non-Small Cell Lung Cancer Cells to X-Ray Exposure Under Chronic Hypoxia.International journal of molecular sciences · 2024Article
- p63 affects distinct metabolic pathways during keratinocyte senescence, evaluated by metabolomic profile and gene expression analysis.Cell death & disease · 2024Article
- Busulfan Chemotherapy Downregulates TAF7/TNF-α Signaling in Male Germ Cell Dysfunction.Biomedicines · 2024Article
- Imaging-guided companion diagnostics in radiotherapy by monitoring APE1 activity with afterglow and MRI imaging.Nature communications · 2024Article
- Mechanism of Apigenin against breast cancer stem cells: network pharmacology and experimental validation.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The tumour suppressor p53 is a nuclear transcription factor with key roles during DNA damage to enable a variety of cellular responses including cell cycle arrest, apoptosis and DNA repair. JMY is an actin nucleator and DNA damage-responsive protein whose sub-cellular localisation is responsive to stress and during DNA damage JMY undergoes nuclear accumulation. To gain an understanding of the wider role for nuclear JMY in transcriptional regulation, we performed transcriptomics to identify JMY-mediated changes in gene expression during the DNA damage response. We show that JMY is required for effective regulation of key p53 target genes involved in DNA repair, including XPC, XRCC5 (Ku80) and TP53I3 (PIG3). Moreover, JMY depletion or knockout leads to increased DNA damage and nuclear JMY requires its Arp2/3-dependent actin nucleation function to promote the clearance of DNA lesions. In human patient samples a lack of JMY is associated with increased tumour mutation count and in cells results in reduced cell survival and increased sensitivity to DNA damage response kinase inhibition. Collectively, we demonstrate that JMY enables p53-dependent DNA repair under genotoxic stress and suggest a role for actin in JMY nuclear activity during the DNA damage response.
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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.