ArticleBiochimie open2016
CRISPR/Cas9-mediated target validation of the splicing inhibitor Pladienolide B.
Article in Biochimie open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed.
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
- Modulation of RNA splicing associated with Wnt signaling pathway using FD-895 and pladienolide B.Aging · 2022Article
- Impaired mRNA splicing and proteostasis in preadipocytes in obesity-related metabolic disease.eLife · 2021Article
- Splicing factors control triple-negative breast cancer cell mitosis through SUN2 interaction and sororin intron retention.Journal of experimental & clinical cancer research : CR · 2021Article
- Splicing factor SF3B1 promotes endometrial cancer progression via regulating KSR2 RNA maturation.Cell death & disease · 2020Article
- Therapeutic approaches to treat human spliceosomal diseases.Current opinion in biotechnology · 2019Review
- Article
- Microbial and Natural Metabolites That Inhibit Splicing: A Powerful Alternative for Cancer Treatment.BioMed research international · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CRISPR/Cas9 system confers molecular immunity in archeal and bacterial species against invading foreign nucleic acids. CRISPR/Cas9 system is used for genome engineering applications across diverse eukaryotic species. In this study, we demonstrate the utility of the CRISPR/Cas9 genome engineering system for drug target validation in human cells. Pladienolide B is a natural macrolide with antitumor activities mediated through the inhibition of pre-mRNA splicing. To validate the spliceosomal target of Pladienolide B, we employed the CRSIPR/Cas9 system to introduce targeted mutations in the subunits of the SF3B complex in the HEK293T cells. Our data reveal that targeted mutagenesis of the SF3b1 subunit exhibited higher levels of resistance to Pladienolide B. Therefore, our data validate the spliceosomal target of Pladienolide B and provide a proof of concept on using the CRISPR/Cas9 system for drug target identification and validation.
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Registered trials
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