ArticleNature communications2018
Widespread intronic polyadenylation diversifies immune cell transcriptomes.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 154 citations in OpenAlex.
- Mechanisms of transcription termination across the coding and noncoding loci of the genome.Nature reviews. Molecular cell biology · 2026Review
- Dynamics of intronic polyadenylation in the hematopoietic lineage and its regulation by DNA methylation.Genome research · 2026Article
- Regulation of gene expression by alternative polyadenylation in health and disease.Nature reviews. Genetics · 2026Review
- Article
- Intronic polyadenylation-derived long noncoding RNA modulates nucleolar integrity and function.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- PolyAseqTrap: a universal tool for genome-wide identification and quantification of polyadenylation sites from different 3' end sequencing data.Genome biology · 2026Article
- The functional landscape of alternative splicing in hematopoietic lineage commitment.Nature communications · 2026Article
- ASTWAS: modeling alternative polyadenylation and SNP effects in kernel-driven TWAS reveal novel genetic associations for complex traits.Briefings in bioinformatics · 2026Article
- TDP-43 loss induces cryptic polyadenylation in ALS/FTD.Nature neuroscience · 2025Article
- RNA Alternative Splicing and Polyadenylation and Regulation of the Glomerular Filtration Barrier.Journal of the American Society of Nephrology : JASN · 2025Article
- IPScan: Detecting novel intronic PolyAdenylation events with RNA-seq data.PLoS computational biology · 2025Article
- Identification of microprotein-coding intronic polyadenylation isoforms and function in genotoxic anticancer drug response.Genome biology · 2025Article
- Computational methods for alternative polyadenylation and splicing in post-transcriptional gene regulation.Experimental & molecular medicine · 2025Review
- RNA epigenetic modifications as dynamic biomarkers in cancer: from mechanisms to clinical translation.Biomarker research · 2025Review
- U1 snRNP regulates alternative promoter activity by inhibiting premature polyadenylation.Molecular cell · 2025Article
- A nuclear RNA degradation code is recognized by PAXT for eukaryotic transcriptome surveillance.Molecular cell · 2025Article
- Gene expression regulation and polyadenylation in ulcerative colitis via long-chain RNA sequencing.BMC genomics · 2025Article
- Impact of rare non-coding variants on human diseases through alternative polyadenylation outliers.Nature communications · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Multiple Forms and Functions of Premature Termination by RNA Polymerase II.Journal of molecular biology · 2025Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Alternative cleavage and polyadenylation (ApA) is known to alter untranslated region (3'UTR) length but can also recognize intronic polyadenylation (IpA) signals to generate transcripts that lose part or all of the coding region. We analyzed 46 3'-seq and RNA-seq profiles from normal human tissues, primary immune cells, and multiple myeloma (MM) samples and created an atlas of 4927 high-confidence IpA events represented in these cell types. IpA isoforms are widely expressed in immune cells, differentially used during B-cell development or in different cellular environments, and can generate truncated proteins lacking C-terminal functional domains. This can mimic ectodomain shedding through loss of transmembrane domains or alter the binding specificity of proteins with DNA-binding or protein-protein interaction domains. MM cells display a striking loss of IpA isoforms expressed in plasma cells, associated with shorter progression-free survival and impacting key genes in MM biology and response to lenalidomide.
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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.