ArticleMolecular and cellular biology2000
Pre-mRNA splicing by the essential Drosophila protein B52: tissue and target specificity.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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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.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- The SR protein B52/SRp55 regulates splicing of the period thermosensitive intron and mid-day siesta in Drosophila.Scientific reports · 2018Article
- SR proteins control a complex network of RNA-processing events.RNA (New York, N.Y.) · 2015Article
- Genome-wide analysis of the maternal-to-zygotic transition in Drosophila primordial germ cells.Genome biology · 2012Article
- The SR protein B52/SRp55 is required for DNA topoisomerase I recruitment to chromatin, mRNA release and transcription shutdown.PLoS genetics · 2010Article
- Article
- DX16 is a novel SR protein phosphorylated by DOA.Molecular and cellular biochemistry · 2008Article
- Identification of RNA binding sequences of Drosophila SR protein DX16.Molecular and cellular biochemistry · 2007Article
- The impact of alternative splicing in vivo: mouse models show the way.RNA (New York, N.Y.) · 2007Review
- Eye development under the control of SRp55/B52-mediated alternative splicing of eyeless.PloS one · 2007Article
- Specific role of the SR protein splicing factor B52 in cell cycle control in Drosophila.Molecular and cellular biology · 2006Article
- Negative feedback regulation among SR splicing factors encoded by Rbp1 and Rbp1-like in Drosophila.The EMBO journal · 2005Article
- A novel role for shuttling SR proteins in mRNA translation.Genes & development · 2004Article
- Dilated cardiomyopathy caused by tissue-specific ablation of SC35 in the heart.The EMBO journal · 2004Article
- Ectopic expression of atRSZ33 reveals its function in splicing and causes pleiotropic changes in development.Molecular biology of the cell · 2003Article
- Mutations in tau gene exon 10 associated with FTDP-17 alter the activity of an exonic splicing enhancer to interact with Tra2 beta.The Journal of biological chemistry · 2003Article
- Specific SR protein-dependent splicing substrates identified through genomic SELEX.Nucleic acids research · 2003Article
- Regulation of alternative splicing by SRrp86 through coactivation and repression of specific SR proteins.RNA (New York, N.Y.) · 2002Article
- SC35 autoregulates its expression by promoting splicing events that destabilize its mRNAs.The EMBO journal · 2001Article
- Functional characterization of SR and SR-related genes in Caenorhabditis elegans.The EMBO journal · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
B52, an essential SR protein of Drosophila melanogaster, stimulates pre-mRNA splicing in splicing-deficient mammalian S100 extracts. Surprisingly, mutant larvae depleted of B52 were found to be capable of splicing at least several pre-mRNAs tested (H. Z. Ring and J. T. Lis, Mol. Cell. Biol. 14:7499-7506, 1994). In a homologous in vitro system, we demonstrated that B52 complements a Drosophila S100 extract to allow splicing of a Drosophila fushi tarazu (ftz) mini-pre-mRNA. Moreover, Kc cell nuclear extracts that were immunodepleted of B52 lost their ability to splice this ftz pre-mRNA. In contrast, splicing of this same ftz pre-mRNA occurred in whole larvae homozygous for the B52 deletion. Other SR protein family members isolated from these larvae could substitute for B52 splicing activity in vitro. We also observed that SR proteins are expressed variably in different larval tissues. B52 is the predominant SR protein in specific tissues, including the brain. Tissues in which B52 is normally the major SR protein, such as larval brain tissue, failed to produce ftz mRNA in the B52 deletion line. These observations support a model in which the lethality of the B52 deletion strain is a consequence of splicing defects in tissues in which B52 is normally the major SR protein.
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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.