ReviewBest practice & research. Clinical haematology2020
Spliceosomal factor mutations and mis-splicing in MDS.
Review in Best practice & research. Clinical haematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Review
- The splicing factor Prpf31 is required for hematopoietic stem and progenitor cell expansion during zebrafish embryogenesis.The Journal of biological chemistry · 2024Article
- The Promising Role of Non-Coding RNAs as Biomarkers and Therapeutic Targets for Leukemia.Genes · 2023Review
- Functional analyses of human LUC7-like proteins involved in splicing regulation and myeloid neoplasms.Cell reports · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic, heterozygous missense and nonsense mutations in at least seven proteins that function in the spliceosome are found at high frequency in MDS patients. These proteins act at various steps in the process of splicing by the spliceosome and lead to characteristic alterations in the alternative splicing of a subset of genes. Several studies have investigated the effects of these mutations and have attempted to identify a commonly affected gene or pathway. Here, we summarize what is known about the normal function of these proteins and how the mutations alter the splicing landscape of the genome. We also summarize the commonly mis-spliced gene targets and discuss the state of mechanistic unification that has been achieved. Finally, we discuss alternative mechanisms by which these mutations may lead to disease.
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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.