The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
RNA splicing factors as oncoproteins and tumour suppressors
Open accessAbstract
The recent genomic characterization of cancers has revealed recurrent somatic point mutations and copy number changes affecting genes encoding RNA splicing factors. Initial studies of these 'spliceosomal mutations' suggest that the proteins bearing these mutations exhibit altered splice site and/or exon recognition preferences relative to their wild-type counterparts, resulting in cancer-specific mis-splicing. Such changes in the splicing machinery may create novel vulnerabilities in cancer cells that can be therapeutically exploited using compounds that can influence the splicing process. Further studies to dissect the biochemical, genomic and biological effects of spliceosomal mutations are crucial for the development of cancer therapies targeted at these mutations.
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Self-citationAryl Sulfonamides Degrade RBM39 and RBM23 by Recruitment to CRL4-DCAF15
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“Nevertheless, when assessed at the level of individual pro- teins, PP2A inhibition almost exclusively increased phosphorylation of cancer-related splicing factors (e.g. HNRNPA1, SRSF3, and RBM4) (47), whereas a distinct set of splicing factors was found to be dephosphorylated upon depletion of the PAIPs (Fig.”
Background
Metadata
- Authors
- Dvinge, H., Kim, E., Abdel-Wahab, O., & Bradley, R. K.
- Venue
- Nature Reviews Cancer
- Published
- 2016-06-10
- Volume
- 16
- Issue
- 7
- Pages
- 413-430
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2410306399
- Cited by
- 687
- References
- 30
- FWCI
- 4.44
- Type
- journal article
- Language
- en
- Open access
- green
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