ArticleNucleic acids research2006
Depletion of SMN by RNA interference in HeLa cells induces defects in Cajal body formation.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 67 citations in OpenAlex.
- Intranucleolar Invasion of Cajal Body Remnants Suppresses Ribosomal Biogenesis inbioRxiv : the preprint server for biology · 2026Article
- Spinal muscular atrophy: Biology, pathogenesis, and therapeutic advances.Therapeutic advances in neurological disorders · 2026Review
- Spinal muscular atrophy in the disease-modifying therapy era: successes, limitations and future directions.Frontiers in molecular medicine · 2026Review
- Biomolecular condensates: molecular structure, biological functions, diseases, and therapeutic targets.Molecular biomedicine · 2025Review
- Dynamic interaction of spliceosomal snRNPs with coilin explains Cajal body characteristics.The Journal of cell biology · 2025Article
- A Novel Role for Coilin in Vertebrate Innate Immunity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Identification of coilin interactors reveals coordinated control of Cajal body number and structure.The Journal of cell biology · 2025Article
- The SMN-ribosome interplay: a new opportunity for Spinal Muscular Atrophy therapies.Biochemical Society transactions · 2024Review
- Coilin and Cajal bodies.Nucleus (Austin, Tex.) · 2023Review
- The intrinsically disordered TSSC4 protein acts as a helicase inhibitor, placeholder and multi-interaction coordinator during snRNP assembly and recycling.Nucleic acids research · 2022Article
- Advances in the phase separation-organized membraneless organelles in cells: a narrative review.Translational cancer research · 2021Review
- Article
- VRK1 (Y213H) homozygous mutant impairs Cajal bodies in a hereditary case of distal motor neuropathy.Annals of clinical and translational neurology · 2020Article
- Diabetic neuropathy and the sensory neuron: New aspects of pathogenesis and their treatment implications.Journal of diabetes investigation · 2018Review
- UsnRNP biogenesis: mechanisms and regulation.Chromosoma · 2017Review
- Review
- SMN - A chaperone for nuclear RNP social occasions?RNA biology · 2017Review
- Diabetic polyneuropathy, sensory neurons, nuclear structure and spliceosome alterations: a role for CWC22.Disease models & mechanisms · 2017Article
- TDRD6 mediates early steps of spliceosome maturation in primary spermatocytes.PLoS genetics · 2017Article
- Coilin: The first 25 years.RNA biology · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal degeneration in spinal muscular atrophy (SMA) is caused by reduced expression of the survival of motor neuron (SMN) protein. The SMN protein is ubiquitously expressed and is present both in the cytoplasm and in the nucleus where it localizes in Cajal bodies. The SMN complex plays an essential role for the biogenesis of spliceosomal U-snRNPs. In this article, we have used an RNA interference approach in order to analyse the effects of SMN depletion on snRNP assembly in HeLa cells. Although snRNP profiles are not perturbed in SMN-depleted cells, we found that SMN depletion gives rise to cytoplasmic accumulation of a GFP-SmB reporter protein. We also demonstrate that the SMN protein depletion induces defects in Cajal body formation with coilin being localized in multiple nuclear foci and in nucleolus instead of canonical Cajal bodies. Interestingly, the coilin containing foci do not contain snRNPs but appear to co-localize with U85 scaRNA. Because Cajal bodies represent the location in which snRNPs undergo 2'-O-methylation and pseudouridylation, our results raise the possibility that SMN depletion might give rise to a defect in the snRNA modification process.
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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.