ArticleMolecular biology of the cell2008
Fas splicing regulation during early apoptosis is linked to caspase-mediated cleavage of U2AF65.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Exploitation of host U2AF1 and U2AF2 splicing factors facilitates mosquito-borne orthoflavivirus infection across species.Nucleic acids research · 2026Article
- The three as: Alternative splicing, alternative polyadenylation and their impact on apoptosis in immune function.Immunological reviews · 2021Review
- Phylogenetic Analysis of the Plant U2 snRNP Auxiliary Factor Large Subunit A Gene Family in Response to Developmental Cues and Environmental Stimuli.Frontiers in plant science · 2021Article
- Alternative splicing of U2AF1 reveals a shared repression mechanism for duplicated exons.Nucleic acids research · 2017Article
- Post-transcriptional Regulation of Immunological Responses through Riboclustering.Frontiers in immunology · 2016Review
- The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.The Journal of biological chemistry · 2014Article
- Post-transcriptional coordination of immunological responses by RNA-binding proteins.Nature immunology · 2014Review
- Long-term reduction of T-cell intracellular antigens leads to increased beta-actin expression.Molecular cancer · 2014Article
- Proteomic analysis of protein expression profiles during hyperthermia-induced apoptosis in Tca8113 cells.Oncology letters · 2013Article
- Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related/like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R.Nucleic acids research · 2010Article
- Depletion of T-cell intracellular antigen proteins promotes cell proliferation.Genome biology · 2009Article
- Interactome for auxiliary splicing factor U2AF(65) suggests diverse roles.Biochimica et biophysica actaArticle
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1 author at 1 institution in 1 country.
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Abstract
U2 small nuclear ribonucleoprotein (snRNP) auxiliary factor 65 kDa (U2AF65) is an essential splicing factor in the recognition of the pre-mRNA 3' splice sites during the assembly of the splicing commitment complex. We report here that U2AF65 is proteolyzed during apoptosis. This cleavage is group I or III caspase dependent in a noncanonical single site localized around the aspartic acid(128) residue and leads to the separation of the N- and C-terminal parts of U2AF65. The U2AF65 N-terminal fragment mainly accumulates in the nucleus within nuclear bodies (nucleoli-like pattern) and to a much lesser extent in the cytoplasm, whereas the C-terminal fragment is found in the cytoplasm, even in localization studies on apoptosis induction. From a functional viewpoint, the N-terminal fragment promotes Fas exon 6 skipping from a reporter minigene, by acting as a dominant-negative version of U2AF65, whereas the C-terminal fragment has no significant effect. The dominant-negative behavior of the U2AF65 N-terminal fragment can be reverted by U2AF35 overexpression. Interestingly, U2AF65 proteolysis in Jurkat cells on induction of early apoptosis correlates with the down-regulation of endogenous Fas exon 6 inclusion. Thus, these results support a functional link among apoptosis induction, U2AF65 cleavage, and the regulation of Fas alternative splicing.
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