Alternative splicing of the TNFSF13B (BAFF) pre-mRNA and expression of the BAFFX1 isoform in human immune cells
Human B cell activating factor (TNFSF13B, BAFF) is a tumor necrosis factor superfamily member. Binding its unique receptor (TNFRSF13C, BAFF-R) mediates gene expression and cell survival in B cells via activation of NFκB pathway. Furthermore, there is data indicating a role in T cell function. A func...
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| Hauptverfasser: | , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
04 August 2020
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| In: |
Gene
Year: 2020, Jahrgang: 760 |
| ISSN: | 1879-0038 |
| DOI: | 10.1016/j.gene.2020.145021 |
| Online-Zugang: | Verlag, Volltext: https://doi.org/10.1016/j.gene.2020.145021 Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0378111920306909 
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| Verfasserangaben: | Patrick Stelmach, Michael Pütz, Robert Pollmann, Michael Happel, Susanne Stei, Kerstin Schlegel, Maria Seipelt, Christian Eienbröker, Rüdiger Eming, Robert Mandic, Magdalena Huber, Björn Tackenberg |
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| 245 | 1 | 0 | |a Alternative splicing of the TNFSF13B (BAFF) pre-mRNA and expression of the BAFFX1 isoform in human immune cells |c Patrick Stelmach, Michael Pütz, Robert Pollmann, Michael Happel, Susanne Stei, Kerstin Schlegel, Maria Seipelt, Christian Eienbröker, Rüdiger Eming, Robert Mandic, Magdalena Huber, Björn Tackenberg |
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| 520 | |a Human B cell activating factor (TNFSF13B, BAFF) is a tumor necrosis factor superfamily member. Binding its unique receptor (TNFRSF13C, BAFF-R) mediates gene expression and cell survival in B cells via activation of NFκB pathway. Furthermore, there is data indicating a role in T cell function. A functionally inhibitory isoform (ΔBAFF) resulting from the deletion of exon 3 in the TNFSF13B pre-RNA has already been reported. However, data on the complexity of post-transcriptional regulation is scarce. Here, we report molecular cloning of nine TNFSF13B transcript variants resulting from alternative splicing of the TNFSF13B pre-mRNA including BAFFX1. This variant is characterized by a partial retention of intron 3 of the TNFSF13B gene causing the appearance of a premature stop codon. We demonstrate the expression of the corresponding BAFFX1 protein in Jurkat T cells, in ex vivo human immune cells and in human tonsillar tissue. Thereby we contribute to the understanding of TNFSF13B gene regulation and reveal that BAFF is regulated through a post-transcriptional mechanism to a greater extent than reported to date. | ||
| 650 | 4 | |a B cell activating factor | |
| 650 | 4 | |a BAFF | |
| 650 | 4 | |a BAFFX1 | |
| 650 | 4 | |a Post-transcriptional modification | |
| 650 | 4 | |a TNFSF13B | |
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| 700 | 1 | |a Schlegel, Kerstin |e VerfasserIn |4 aut | |
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