ArticleGenes & development2018
Loss of
Article in Genes & development, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Targeting the Lin28/let-7 Axis with Compounds to Regulate Transcriptional Control in Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- Ribonucleases in Mendelian disease: Characterization and insight from model organisms.Genes & diseases · 2025Review
- Three Siblings With an Attenuated Presentation of Perlman Syndrome: A Case Report and Literature Review.Molecular genetics & genomic medicine · 2025Review
- Dis3l2 is essential for neural crest survival by modulating Akt signaling.Cell communication and signaling : CCS · 2025Article
- RNA Editors Sculpt the Transcriptome During Terminal Erythropoiesis.Research square · 2025Article
- DIS3L, cytoplasmic exosome catalytic subunit, is essential for development but not cell viability in mice.RNA (New York, N.Y.) · 2025Article
- Regulating Protein-RNA Interactions: Advances in Targeting the LIN28/Let-7 Pathway.International journal of molecular sciences · 2024Review
- Conditional ablation of DIS3L2 ribonuclease in pre-meiotic germ cells causes defective spermatogenesis and infertility in male mice.Theranostics · 2024Article
- DIS3L2 knockdown impairs key oncogenic properties of colorectal cancer cells via the mTOR signaling pathway.Cellular and molecular life sciences : CMLS · 2023Article
- A shape-shifting nuclease unravels structured RNA.Nature structural & molecular biology · 2023Article
- Recent findings on the role of microRNAs in genetic kidney diseases.Molecular biology reports · 2022Review
- Review
- Loss of RTN3 phenocopies chronic kidney disease and results in activation of the IGF2-JAK2 pathway in proximal tubular epithelial cells.Experimental & molecular medicine · 2022Article
- Post-transcriptional regulation in spermatogenesis: all RNA pathways lead to healthy sperm.Cellular and molecular life sciences : CMLS · 2021Review
- Up-to-date on the evidence linking miRNA-related epitranscriptomic modifications and disease settings. Can these modifications affect cross-kingdom regulation?RNA biology · 2021Article
- Research advances in the targeted therapy and immunotherapy of Wilms tumor: a narrative review.Translational cancer research · 2021Review
- A stress-induced tyrosine-tRNA depletion response mediates codon-based translational repression and growth suppression.The EMBO journal · 2021Article
- Editing and Chemical Modifications on Non-Coding RNAs in Cancer: A New Tale with Clinical Significance.International journal of molecular sciences · 2021Review
- Dis3L2 regulates cell proliferation and tissue growth through a conserved mechanism.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Loss of function of the DIS3L2 exoribonuclease is associated with Wilms tumor and the Perlman congenital overgrowth syndrome. LIN28, a Wilms tumor oncoprotein, triggers the DIS3L2-mediated degradation of the precursor of let-7, a microRNA that inhibits Wilms tumor development. These observations have led to speculation that DIS3L2-mediated tumor suppression is attributable to let-7 regulation. Here we examine new DIS3L2-deficient cell lines and mouse models, demonstrating that DIS3L2 loss has no effect on mature let-7 levels. Rather, analysis of
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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.