ArticleJournal of cell science2016
DICER, DROSHA and DNA damage response RNAs are necessary for the secondary recruitment of DNA damage response factors.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed, 145 citations in OpenAlex.
- DDX3X regulates DNA repair pathway choice at double-strand breaks via RNA-DNA hybrid formation.Cell death and differentiation · 2026Article
- Therapeutic inhibition of telomeric DNA damage response rescues hematopoietic dysfunction driven by telomere shortening and aging.Nature aging · 2026Article
- Dual roles of the DHX9 RGG domain in hybrid-dependent recruitment and suppression of 53BP1.Scientific reports · 2026Article
- Proteasomal-dependent CHK1 degradation leads to DNA damage accumulation in ALS cellular model systems.Cell death & disease · 2026Article
- Non-coding RNA regulation of the radiation-induced DNA damage response and its translational relevance.Discover oncology · 2026Review
- DNA damage response defects induced by the formation of TDP-43 and mutant FUS cytoplasmic inclusions and their pharmacological rescue.Cell death and differentiation · 2025Article
- The multiple layers of RNA response in double-strand break repair.Experimental & molecular medicine · 2025Review
- Article
- NSUN2 facilitates DICER cleavage of DNA damage-associated R-loops to promote repair.Nature communications · 2025Article
- DICER1: The Argonaute Endonuclease Family Member and Its Role in Pediatric and Youth Pathology.Biology · 2025Review
- Traffic light at DSB-transit regulation between gene transcription and DNA repair.FEBS letters · 2025Review
- Tetrameric INTS6-SOSS1 complex facilitates DNA:RNA hybrid autoregulation at double-strand breaks.Nucleic acids research · 2024Article
- NEK1 haploinsufficiency worsens DNA damage, but not defective ciliogenesis, in C9ORF72 patient-derived iPSC-motoneurons.Human molecular genetics · 2024Article
- Understanding the Dosage-Dependent Role ofInternational journal of molecular sciences · 2024Article
- Article
- SARS-CoV-2 N protein-induced Dicer, XPO5, SRSF3, and hnRNPA3 downregulation causes pneumonia.Nature communications · 2024Article
- The GATAD2B-NuRD complex drives DNA:RNA hybrid-dependent chromatin boundary formation upon DNA damage.The EMBO journal · 2024Article
- KDM7A-DT induces genotoxic stress, tumorigenesis, and progression of p53 missense mutation-associated invasive breast cancer.Frontiers in oncology · 2024Article
- USP7 reduces the level of nuclear DICER, impairing DNA damage response and promoting cancer progression.Molecular oncology · 2024Article
- Break-induced RNA-DNA hybrids (BIRDHs) in homologous recombination: friend or foe?EMBO reports · 2023Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The DNA damage response (DDR) plays a central role in preserving genome integrity. Recently, we reported that the endoribonucleases DICER and DROSHA contribute to DDR activation by generating small non-coding RNAs, termed DNA damage response RNA (DDRNA), carrying the sequence of the damaged locus. It is presently unclear whether DDRNAs act by promoting the primary recognition of DNA lesions or the secondary recruitment of DDR factors into cytologically detectable foci and consequent signal amplification. Here, we demonstrate that DICER and DROSHA are dispensable for primary recruitment of the DDR sensor NBS1 to DNA damage sites. Instead, the accumulation of the DDR mediators MDC1 and 53BP1 (also known as TP53BP1), markers of secondary recruitment, is reduced in DICER- or DROSHA-inactivated cells. In addition, NBS1 (also known as NBN) primary recruitment is resistant to RNA degradation, consistent with the notion that RNA is dispensable for primary recognition of DNA lesions. We propose that DICER, DROSHA and DDRNAs act in the response to DNA damage after primary recognition of DNA lesions and, together with γH2AX, are essential for enabling the secondary recruitment of DDR factors and fuel the amplification of DDR signaling.
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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.