SPF45/RBM17-dependent splicing and multidrug resistance to cancer chemotherapy
- 2 November 2021
- journal article
- editorial
- Published by Taylor & Francis in Molecular & Cellular Oncology
- Vol. 8 (6) , 1996318
Abstract
The early splicing complex A occupies at least eighty nucleotides of intron, in which U2AF covers the polypyrimidine tract. SPF45 (RBM17) functionally substitutes for U2AF on a subset of short introns. Since SPF45 expression confers resistance to various anticancer drugs, SPF45-dependent splicing may play a critical role in multidrug resistance.Keywords
Funding Information
- Grants-in-Aid for Scientific Research (JP18K07304)
- Japan Society for the Promotion of Science
- Hori Sciences and Arts Foundation, and a Research
- Grants-in-Aid for Scientific Research (JP16H04705)
- Challenging Exploratory Research (JP16K14659)
This publication has 14 references indexed in Scilit:
- Extensive cryptic splicing upon loss of RBM17 and TDP43 in neurodegeneration modelsHuman Molecular Genetics, 2016
- Identification and Validation of Evolutionarily Conserved Unusually Short Pre-mRNA Introns in the Human GenomeInternational Journal of Molecular Sciences, 2015
- Phosphorylation of the alternative mRNA splicing factor 45 (SPF45) by Clk1 regulates its splice site utilization, cell migration and invasionNucleic Acids Research, 2013
- Mechanistic insights into human pre-mRNA splicing of human ultra-short introns: Potential unusual mechanism identifies G-rich intronsBiochemical and Biophysical Research Communications, 2012
- The Spliceosome: Design Principles of a Dynamic RNP MachineCell, 2009
- U2AF-homology motif interactions are required for alternative splicing regulation by SPF45Nature Structural & Molecular Biology, 2007
- Human Splicing Factor SPF45 (RBM17) Confers Broad Multidrug Resistance to Anticancer Drugs When Overexpressed— a Phenotype Partially Reversed By Selective Estrogen Receptor ModulatorsCancer Research, 2005
- Human SPF45, a Splicing Factor, Has Limited Expression in Normal Tissues, Is Overexpressed in Many Tumors, and Can Confer a Multidrug-Resistant Phenotype to CellsThe American Journal of Pathology, 2003
- Splicing Regulation at the Second Catalytic Step by Sex-lethal Involves 3′ Splice Site Recognition by SPF45Cell, 2002
- Resistance to anticancer drugs in NIH3T3 cells transfected with c-myc and/or c-H-ras genesBritish Journal of Cancer, 1991