ArticleThe Journal of cell biology1997
Targeting of U2AF65 to sites of active splicing in the nucleus.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 125 citations in OpenAlex.
- U2AF2 controls alternative splicing in speckle-proximal regions in an RS domain-dependent manner.Nucleic acids research · 2026Article
- Chromatin-bound U2AF2 splicing factor ensures exon inclusion.Molecular cell · 2025Article
- Construction of a proximity labeling vector to identify protein-protein interactions in human stem cells.PloS one · 2025Article
- Identification of a 5-gene signature panel for the prediction of prostate cancer progression.British journal of cancer · 2024Article
- A presumed missense variant in the U2AF2 gene causes exon skipping in neurodevelopmental diseases.Journal of human genetics · 2023Review
- Splicing factor USP39 promotes ovarian cancer malignancy through maintaining efficient splicing of oncogenic HMGA2.Cell death & disease · 2021Article
- 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
- Article
- U2AFEMBO reports · 2019Article
- Low-density lipoprotein receptor-related protein 6 regulates alternative pre-mRNA splicing.Journal of cellular and molecular medicine · 2018Article
- Stoichiometries of U2AF35, U2AF65 and U2 snRNP reveal new early spliceosome assembly pathways.Nucleic acids research · 2017Article
- An extended U2AF(65)-RNA-binding domain recognizes the 3' splice site signal.Nature communications · 2016Article
- RNA structure replaces the need for U2AF2 in splicing.Genome research · 2016Article
- Article
- The nuclear cap-binding complex interacts with the U4/U6·U5 tri-snRNP and promotes spliceosome assembly in mammalian cells.RNA (New York, N.Y.) · 2013Article
- Cellular ontogeny of RBMY during human spermatogenesis and its role in sperm motility.Journal of biosciences · 2013Article
- Intron retention in the alternatively spliced region of RON results from weak 3' splice site recognition.PloS one · 2013Article
- Spliceosomal gene mutations are frequent events in the diverse mutational spectrum of chronic myelomonocytic leukemia but largely absent in juvenile myelomonocytic leukemia.Haematologica · 2013Article
- Triplex DNA-binding proteins are associated with clinical outcomes revealed by proteomic measurements in patients with colorectal cancer.Molecular cancer · 2012Article
- The FF4 and FF5 domains of transcription elongation regulator 1 (TCERG1) target proteins to the periphery of speckles.The Journal of biological chemistry · 2012Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
U2AF65 is an essential splicing factor that promotes binding of U2 small nuclear (sn)RNP at the pre-mRNA branchpoint. Here we describe a novel monoclonal antibody that reacts specifically with U2AF65. Using this antibody, we show that U2AF65 is diffusely distributed in the nucleoplasm with additional concentration in nuclear speckles, which represent subnuclear compartments enriched in splicing snRNPs and other splicing factors. Furthermore, transient expression assays using epitope-tagged deletion mutants of U2AF65 indicate that targeting of the protein to nuclear speckles is not affected by removing either the RNA binding domain, the RS domain, or the region required for interaction with U2AF35. The association of U2AF65 with speckles persists during mitosis, when transcription and splicing are downregulated. Moreover, U2AF65 is localized to nuclear speckles in early G1 cells that were treated with transcription inhibitors during mitosis, suggesting that the localization of U2AF65 in speckles is independent of the presence of pre-mRNA in the nucleus, which is consistent with the idea that speckles represent storage sites for inactive splicing factors. After adenovirus infection, U2AF65 redistributes from the speckles and is prefferentially detected at sites of viral transcription. By combining adenoviral infection with transient expression of deletion mutants, we show a specific requirement of the RS domain for recruitment of U2AF65 to sites of active splicing in the nucleus. This suggests that interactions involving the RS region of U2AF65 may play an important role in targeting this protein to spliceosomes in vivo.
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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.