ArticleJournal of molecular neuroscience : MN2011
PSF suppresses tau exon 10 inclusion by interacting with a stem-loop structure downstream of exon 10.
Article in Journal of molecular neuroscience : MN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Overexpression of SFPQ Improves Cognition and Memory in AD Mice.Neural plasticity · 2025Article
- Cooperative nuclear action of RNA-binding proteins PSF and G3BP2 to sustain neuronal cell viability is decreased in aging and dementia.Aging cell · 2024Article
- Role of RNA binding proteins of theRNA biology · 2024Review
- Alternative splicing in neurodegenerative disease and the promise of RNA therapies.Nature reviews. Neuroscience · 2023Review
- Identification of small-molecule inhibitors against the interaction of RNA-binding protein PSF and its target RNA for cancer treatment.PNAS nexus · 2023Article
- Prematurely terminated intron-retaining mRNAs invade axons in SFPQ null-driven neurodegeneration and are a hallmark of ALS.Nature communications · 2022Article
- Article
- SFPQ-ABL1 and BCR-ABL1 use different signaling networks to drive B-cell acute lymphoblastic leukemia.Blood advances · 2022Article
- Alternative splicing in Alzheimer's disease.Aging clinical and experimental research · 2021Review
- A conserved role for the ALS-linked splicing factor SFPQ in repression of pathogenic cryptic last exons.Nature communications · 2021Article
- Murine Long Noncoding RNA Morrbid Contributes in the Regulation of NRAS Splicing in Hepatocytes In Vitro.International journal of molecular sciences · 2020Article
- Spectrum of tau pathologies in Huntington's disease.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Identification of conserved, primary sequence motifs that direct retrovirus RNA fate.Nucleic acids research · 2018Article
- Exploitation of nuclear functions by human rhinovirus, a cytoplasmic RNA virus.PLoS pathogens · 2018Article
- Non-nuclear Pool of Splicing Factor SFPQ Regulates Axonal Transcripts Required for Normal Motor Development.Neuron · 2017Article
- The DBHS proteins SFPQ, NONO and PSPC1: a multipurpose molecular scaffold.Nucleic acids research · 2016Article
- Microtubule-Tau Interaction as a Therapeutic Target for Alzheimer's Disease.Journal of molecular neuroscience : MN · 2016Review
- Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis.Parkinson's disease · 2016Article
- Comparison of the neuropsychological mechanisms of 2,6-diisopropylphenol and N-methyl-D-aspartate receptor antagonist against electroconvulsive therapy-induced learning and memory impairment in depressed rats.Molecular medicine reports · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Microtubule binding protein Tau has been implicated in a wide range of neurodegenerative disorders collectively classified as tauopathies. Exon 10 of the human tau gene, which codes for a microtubule binding repeat region, is alternatively spliced to form Tau protein isoforms containing either four or three microtubule binding repeats, Tau4R and Tau3R, respectively. The levels of different Tau splicing isoforms are fine-tuned by alternative splicing with the ratio of Tau4R/Tau3R maintained approximately at one in adult neurons. Mutations that disrupt tau exon 10 splicing regulation cause an imbalance of different tau splicing isoforms and have been associated with tauopathy. To search for factors interacting with tau pre-messenger RNA (pre-mRNA) and regulating tau exon 10 alternative splicing, we performed a yeast RNA-protein interaction screen and identified polypyrimidine tract binding protein associated splicing factor (PSF) as a candidate tau exon 10 splicing regulator. UV crosslinking experiments show that PSF binds to the stem-loop structure at the 5' splice site downstream of tau exon 10. This PSF-interacting RNA element is distinct from known PSF binding sites previously identified in other genes. Overexpression of PSF promotes tau exon 10 exclusion, whereas down-regulation of the endogenous PSF facilitates exon 10 inclusion. Immunostaining shows that PSF is expressed in the human brain regions affected by tauopathy. Our data reveal a new player in tau exon 10 alternative splicing regulation and uncover a previously unknown mechanism of PSF in regulating tau pre-mRNA splicing.
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Registered trials
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