ArticleProceedings of the National Academy of Sciences of the United States of America2015
hnRNP U protein is required for normal pre-mRNA splicing and postnatal heart development and function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 125 citations in OpenAlex.
- SAF-A/HNRNPU regulates euchromatin dynamics and is required for nuclear envelope integrity.bioRxiv : the preprint server for biology · 2026Article
- RNA splicing and cardiovascular disease: a guide for cardiologists.European heart journal · 2026Review
- HNRNPU mutations redirect cell cycle control to E2F in MYC-driven lymphomas.Blood advances · 2026Article
- The Calmodulin/Striatin Interaction Is Enhanced in Diabetic Hearts and Defines Novel Signaling Clusters Implicated in Cardiac Remodeling.ACS omega · 2026Article
- Structural variants in human congenital heart disease disrupt distal genomic regulatory contacts of developmental genes.bioRxiv : the preprint server for biology · 2026Article
- Molecular interactome of HNRNPU reveals regulatory networks in neuronal differentiation and DNA methylation.Nucleic acids research · 2026Article
- hnRNPU Safeguards Oocyte Development and Female Fertility via Regulation of Alternative Splicing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- SNORA49 negatively regulates self-renewal of liver cancer stem cells and hepatocarcinogenesis via suppressing SOX9 transcription.Nature communications · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Splicing as an integrative layer linking cell cycle regulation, epigenetic dynamics, and environmental responses in plants.Frontiers in plant science · 2026Review
- LAP2 Isoform Profile in Heart Ageing and in Cardiac Cell Proliferation and Differentiation: Input From CRISPR-Cas9-mediated LAP2a Knockdown in H9C2.International journal of medical sciences · 2026Article
- Role of the SAF-A/HNRNPU ATPase and RGG domains in X chromosome inactivation, nuclear dynamics, transcription, splicing, and cell proliferation.bioRxiv : the preprint server for biology · 2025Article
- Surviving desiccation: key factors underlying tolerance in prokaryotes and eukaryotes.Protoplasma · 2025Review
- Decoding Cardiac Maturation Program: Insights from RNA Splicing Regulation.Current cardiology reports · 2025Review
- Alternative splicing in stem cells and development: research progress and emerging technologies.Cell regeneration (London, England) · 2025Review
- Role of the SAF-A/HNRNPU SAP domain in X chromosome inactivation, nuclear dynamics, transcription, splicing, and cell proliferation.PLoS genetics · 2025Article
- RNA G-quadruplexes control mitochondria-localized mRNA translation and energy metabolism.Nature communications · 2025Article
- The nuclear matrix stabilizes primed-specific genes in human pluripotent stem cells.Nature cell biology · 2025Article
- Developmental and Epileptic Encephalopathy: Pathogenesis of Intellectual Disability Beyond Channelopathies.Biomolecules · 2025Review
- Transcriptomic Alterations in Spliceosome Components in Advanced Heart Failure: Status of Cardiac-Specific Alternative Splicing Factors.International journal of molecular sciences · 2024Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
We report that mice lacking the heterogeneous nuclear ribonucleoprotein U (hnRNP U) in the heart develop lethal dilated cardiomyopathy and display numerous defects in cardiac pre-mRNA splicing. Mutant hearts have disorganized cardiomyocytes, impaired contractility, and abnormal excitation-contraction coupling activities. RNA-seq analyses of Hnrnpu mutant hearts revealed extensive defects in alternative splicing of pre-mRNAs encoding proteins known to be critical for normal heart development and function, including Titin and calcium/calmodulin-dependent protein kinase II delta (Camk2d). Loss of hnRNP U expression in cardiomyocytes also leads to aberrant splicing of the pre-mRNA encoding the excitation-contraction coupling component Junctin. We found that the protein product of an alternatively spliced Junctin isoform is N-glycosylated at a specific asparagine site that is required for interactions with specific protein partners. Our findings provide conclusive evidence for the essential role of hnRNP U in heart development and function and in the regulation of alternative splicing.
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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.