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J Biol Chem. 2018 Jun 29;293(26):10235-10244. doi: 10.1074/jbc.RA117.001349. Epub 2018 May 17.

FOXP3 interacts with hnRNPF to modulate pre-mRNA alternative splicing.

Author information

1
From the Wells Center for Pediatric Research and Department of Pediatrics and.
2
Benaroya Research Institute at Virginia Mason, Seattle, Washington 98101.
3
From the Wells Center for Pediatric Research and Department of Pediatrics and zhoub@iu.edu.
4
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana 46202 and.

Abstract

FOXP3 promotes the development and function of regulatory T cells mainly through regulating the transcription of target genes. RNA alternative splicing has been implicated in a wide range of physiological and pathophysiological processes. We report here that FOXP3 associates with heterogeneous nuclear ribonucleoprotein (hnRNP) F through the exon 2-encoded region of FOXP3 and the second quasi-RNA recognition motif (qRRM) of hnRNPF. FOXP3 represses the ability of hnRNPF to bind to its target pre-mRNA and thus modulates RNA alternative splicing. Furthermore, overexpression of mouse hnRNPF in in vitro-differentiated regulatory T cells (Tregs) reduced their suppressive function. Thus, our studies identify a novel mechanism by which FOXP3 regulates mRNA alternative splicing to modulate the function of regulatory T cells.

KEYWORDS:

RNA splicing; RNA-protein interaction; Treg; alternative splicing; forkhead box P3 (FOXP3); heterogeneous nuclear ribonucleoprotein (hnRNP); immunology; immunosuppression

PMID:
29773655
PMCID:
PMC6028976
[Available on 2019-06-29]
DOI:
10.1074/jbc.RA117.001349

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