ArticleRNA (New York, N.Y.)2009
The conserved 3' end domain of U6atac snRNA can direct U6 snRNA to the minor spliceosome.
Article in RNA (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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
8 citing papers in PubMed, 10 citations in OpenAlex.
- RNA Polymerase III-Transcribed RNAs in Health and Disease: Mechanisms, Dysfunction, and Future Directions.International journal of molecular sciences · 2025Review
- Clinical interpretation of variants identified in RNU4ATAC, a non-coding spliceosomal gene.PloS one · 2020Article
- The life of U6 small nuclear RNA, from cradle to grave.RNA (New York, N.Y.) · 2018Review
- Mutations in the U11/U12-65K protein associated with isolated growth hormone deficiency lead to structural destabilization and impaired binding of U12 snRNA.RNA (New York, N.Y.) · 2018Article
- U6atac snRNA stem-loop interacts with U12 p65 RNA binding protein and is functionally interchangeable with the U12 apical stem-loop III.Scientific reports · 2016Article
- Functionally important structural elements of U12 snRNA.Nucleic acids research · 2011Article
- The Pol III transcriptome: Basic features, recurrent patterns, and emerging roles in cancer.Wiley interdisciplinary reviews. RNAReview
- The significant other: splicing by the minor spliceosome.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
U6 and U6atac snRNAs play analogous critical roles in the major U2-dependent and minor U12-dependent spliceosomes, respectively. Previous results have shown that most of the functional cores of these two snRNAs are either highly similar in sequence or functionally interchangeable. Thus, a mechanism must exist to restrict each snRNA to its own spliceosome. Here we show that a chimeric U6 snRNA containing the unique and highly conserved 3' end domain of U6atac snRNA is able to function in vivo in U12-dependent spliceosomal splicing. Function of this chimera required the coexpression of a modified U4atac snRNA; U4 snRNA could not substitute. Partial deletions of this element in vivo, as well as in vitro antisense experiments, showed that the 3' end domain of U6atac snRNA is necessary to direct the U4atac/U6atac.U5 tri-snRNP to the forming U12-dependent spliceosome. In vitro experiments also uncovered a role for U4atac snRNA in this targeting.
Indexed as
Identifiers
What OpenQuestion holds
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.