First Author | Du J | Year | 2018 |
Journal | J Biol Chem | Volume | 293 |
Issue | 26 | Pages | 10235-10244 |
PubMed ID | 29773655 | Mgi Jnum | J:264535 |
Mgi Id | MGI:6196909 | Doi | 10.1074/jbc.RA117.001349 |
Citation | Du J, et al. (2018) FOXP3 interacts with hnRNPF to modulate pre-mRNA alternative splicing. J Biol Chem 293(26):10235-10244 |
abstractText | 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. |