ArticleMolecular cell2020
Antisense-Mediated Transcript Knockdown Triggers Premature Transcription Termination.
Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 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
97 citing papers in PubMed, 144 citations in OpenAlex.
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- Single-cell TimeLapse-seq reveals MTA is an essential retrotransposon orchestrating mouse zygotic genome activation.Nature communications · 2026Article
- RNA-independent cis-autoregulatory circuits within bidirectional gene pairs control metabolism.Science advances · 2026Article
- ESCRT-I complex enhances therapeutic efficacy of ASO drugs by regulating endosomal escape and glucose homeostasis.Molecular therapy. Nucleic acids · 2026Article
- A targeted mutational strategy aiding in generating antisense RNA to knockdown theJournal of bacteriology · 2026Article
- Allele-specific chromatin architecture shapes imprinted domains and coordinates a distal enhancer and antisense transcription at the mouse Mest-Copg2 domain.Nature communications · 2026Article
- Direct roles of long non-coding RNAs in transcription activation.Nature structural & molecular biology · 2026Review
- SNHG10 promotes tumorigenesis through the EGFR/AKT/ERK/mTOR and miR-150-5p/VEGF-A axis, along with gemcitabine resistance in pancreatic ductal adenocarcinoma.Cell death discovery · 2026Article
- Article
- Allelic chromatin structure is a pervasive feature of imprinted domains and functions cooperatively with cis-acting long non-coding RNAs.bioRxiv : the preprint server for biology · 2025Article
- RNA diagnostics and therapeutics: a comprehensive review.RNA biology · 2025Review
- Suppression of Huntington's Disease Somatic Instability by Transcriptional Repression and Direct CAG Repeat Binding.Nature communications · 2025Article
- Off-pore Nucleoporin sPOM121 Transcriptionally Propels β-Catenin-driven Tumor Progression and Immune Escape in Prostate Cancer.Cancer discovery · 2025Article
- Dual roles of DEAD-box RNA helicase Brr2 in genome stability regulation.Nature communications · 2025Article
- Angelman syndrome patient-derived neuron screen leads to clinical ASO rugonersen targeting UBE3A-ATS with long-lasting effect in monkeys.Nucleic acids research · 2025Article
- The landscape of long noncoding RNA during cutaneous squamous cell carcinoma progression.The British journal of dermatology · 2025Article
- Inhibition of the LINE1-derivedMolecular therapy. Nucleic acids · 2025Article
- An ultraconserved snoRNA-like element in long noncoding RNA CRNDE promotes ribosome biogenesis and cell proliferation.Molecular cell · 2025Article
- Development of LncRNA Biomarkers in Extracellular Vesicle of Amniotic Fluid Associated with Antenatal Hydronephrosis.Biomedicines · 2025Article
- CASCADES, a novel SOX2 super-enhancer-associated long noncoding RNA, regulates cancer stem cell specification and differentiation in glioblastoma.Molecular oncology · 2025Article
37 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Antisense oligonucleotides (ASOs) that trigger RNase-H-mediated cleavage are commonly used to knock down transcripts for experimental or therapeutic purposes. In particular, ASOs are frequently used to functionally interrogate long noncoding RNAs (lncRNAs) and discriminate lncRNA loci that produce functional RNAs from those whose activity is attributable to the act of transcription. Transcription termination is triggered by cleavage of nascent transcripts, generally during polyadenylation, resulting in degradation of the residual RNA polymerase II (Pol II)-associated RNA by XRN2 and dissociation of elongating Pol II. Here, we show that ASOs act upon nascent transcripts and, consequently, induce premature transcription termination downstream of the cleavage site in an XRN2-dependent manner. Targeting the transcript 3' end with ASOs, however, allows transcript knockdown while preserving Pol II association with the gene body. These results demonstrate that the effects of ASOs on transcription must be considered for appropriate experimental and therapeutic use of these reagents.
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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.