ArticlePLoS genetics2013
ATM-dependent MiR-335 targets CtIP and modulates the DNA damage response.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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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.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Mapping the non-coding RNA landscape in ataxia telangiectasia: a scoping review of ATM dependent miRNA and lncRNA dysregulation.Molecular biology reports · 2025Article
- MicroRNAs in the abscopal effect: bridging radiotherapy and systemic anti-tumor immunity for enhanced cancer therapy.Clinical & experimental metastasis · 2025Review
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- Transcriptome analysis of liver and ileum reveals potential regulation of long non-coding RNA in pigs with divergent feed efficiency.Animal bioscience · 2025Article
- Review
- Radiation-induced liver disease: beyond DNA damage.Cell cycle (Georgetown, Tex.) · 2023Review
- Interactions between miRNAs and Double-Strand Breaks DNA Repair Genes, Pursuing a Fine-Tuning of Repair.International journal of molecular sciences · 2022Review
- Review
- Home and Away: The Role of Non-Coding RNA in Intracellular and Intercellular DNA Damage Response.Genes · 2021Review
- A Peptide-Nucleic Acid Targeting miR-335-5p Enhances Expression of Cystic Fibrosis Transmembrane Conductance Regulator (Biomedicines · 2021Article
- Jack of all trades? The versatility of RNA in DNA double-strand break repair.Essays in biochemistry · 2020Review
- Current Smoking is Associated with Decreased Expression of miR-335-5p in Parenchymal Lung Fibroblasts.International journal of molecular sciences · 2019Article
- Regulation of DNA Double-Strand Break Repair by Non-Coding RNAs.Molecules (Basel, Switzerland) · 2018Review
- microRNA-mediated differential expression of TRMU, GTPBP3 and MTO1 in cell models of mitochondrial-DNA diseases.Scientific reports · 2017Article
- Sp1-mediated transcriptional activation of miR-205 promotes radioresistance in esophageal squamous cell carcinoma.Oncotarget · 2017Article
- Diverse roles of miR-335 in development and progression of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- DNA damage responsive miR-33b-3p promoted lung cancer cells survival and cisplatin resistance by targeting p21Cell cycle (Georgetown, Tex.) · 2016Article
- Understanding the CREB1-miRNA feedback loop in human malignancies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Diverse microRNAs with convergent functions regulate tumorigenesis.Oncology letters · 2016Article
- miR-19, a component of the oncogenic miR-17∼92 cluster, targets the DNA-end resection factor CtIP.Oncogene · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
ATM plays a critical role in cellular responses to DNA double-strand breaks (DSBs). We describe a new ATM-mediated DSB-induced DNA damage response pathway involving microRNA (miRNA): irradiation (IR)-induced DSBs activate ATM, which leads to the downregulation of miR-335, a miRNA that targets CtIP, which is an important trigger of DNA end resection in homologous recombination repair (HRR). We demonstrate that CREB is responsible for a large portion of miR-335 expression by binding to the promoter region of miR-335. CREB binding is greatly reduced after IR, corroborating with previous studies that IR-activated ATM phosphorylates CREB to reduce its transcription activity. Overexpression of miR-335 in HeLa cells resulted in reduced CtIP levels and post-IR colony survival and BRCA1 foci formation. Further, in two patient-derived lymphoblastoid cell lines with decreased post-IR colony survival, a "radiosensitive" phenotype, we demonstrated elevated miR-335 expression, reduced CtIP levels, and reduced BRCA1 foci formation. Colony survival, BRCA1 foci, and CtIP levels were partially rescued by miRNA antisense AMO-miR-335 treatment. Taken together, these findings strongly suggest that an ATM-dependent CREB-miR-335-CtIP axis influences the selection of HRR for repair of certain DSB lesions.
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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.