scholarly journals The Alternative Splicing Factor, MBNL1, Inhibits Glioblastoma Tumor Initiation and Progression by Reducing Hypoxia-Induced Stemness

2020 ◽  
Vol 80 (21) ◽  
pp. 4681-4692
Author(s):  
Dillon M. Voss ◽  
Anthony Sloan ◽  
Raffaella Spina ◽  
Heather M. Ames ◽  
Eli E. Bar
Keyword(s):  
Alternative Splicing ◽  
Splicing Factor ◽  
Tumor Initiation ◽  
Alternative Splicing Factor

scholarly journals Upregulation of the alternative splicing factor NOVA2 in colorectal cancer vasculature

2018 ◽  
Vol Volume 11 ◽  
pp. 6049-6056 ◽  
Author(s):  
Stefania Gallo ◽  
Maria Vittoria Arcidiacono ◽  
Veronica Tisato ◽  
Roberta Piva ◽  
Letizia Penolazzi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Alternative Splicing ◽  
Splicing Factor ◽  
Alternative Splicing Factor

scholarly journals Up-regulation of the ubiquitous alternative splicing factor Tra2β causes inclusion of a germ cell-specific exon

2005 ◽  
Vol 14 (16) ◽  
pp. 2289-2303 ◽  
Author(s):  
Julian P. Venables ◽  
Cyril F. Bourgeois ◽  
Caroline Dalgliesh ◽  
Liliane Kister ◽  
James Stevenin ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Germ Cell ◽  
Splicing Factor ◽  
Alternative Splicing Factor

scholarly journals SIAH1 targets the alternative splicing factor T-STAR for degradation by the proteasome

2004 ◽  
Vol 13 (14) ◽  
pp. 1525-1534 ◽  
Author(s):  
Julian P. Venables ◽  
Caroline Dalgliesh ◽  
Maria Paolo Paronetto ◽  
Lindi Skitt ◽  
Jared K. Thornton ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Splicing Factor ◽  
Alternative Splicing Factor

scholarly journals Processive phosphorylation of alternative splicing factor/splicing factor 2

2003 ◽  
Vol 100 (22) ◽  
pp. 12601-12606 ◽  
Author(s):  
B. E. Aubol ◽  
S. Chakrabarti ◽  
J. Ngo ◽  
J. Shaffer ◽  
B. Nolen ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Splicing Factor ◽  
Alternative Splicing Factor

scholarly journals Phosphorylation status of the Kep1 protein alters its affinity for its protein binding partner alternative splicing factor ASF/SF2

2006 ◽  
Vol 400 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Cécile Robard ◽  
Alex Daviau ◽  
Marco Di Fruscio
Keyword(s):  
Alternative Splicing ◽  
Protein Binding ◽  
Cell Line ◽  
Topoisomerase I ◽  
Target Genes ◽  
Rna Binding ◽  
Splicing Factor ◽  
Alternatively Spliced ◽  
Alternative Splicing Factor

Mutations in the Drosophila kep1 gene, encoding a single maxi KH (K homology) domain-containing RNA-binding protein, result in a reduction of fertility in part due to the disruption of the apoptotic programme during oogenesis. This disruption is concomitant with the appearance of an alternatively spliced mRNA isoform encoding the inactive caspase dredd. We generated a Kep1 antibody and have found that the Kep1 protein is present in the nuclei of both the follicle and nurse cells during all stages of Drosophila oogenesis. We have shown that the Kep1 protein is phosphorylated in ovaries induced to undergo apoptosis following treatment with the topoisomerase I inhibitor camptothecin. We have also found that the Kep1 protein interacts specifically with the SR (serine/arginine-rich) protein family member ASF/SF2 (alternative splicing factor/splicing factor 2). This interaction is independent of the ability of Kep1 to bind RNA, but is dependent on the phosphorylation of the Kep1 protein, with the interaction between Kep1 and ASF/SF2 increasing in the presence of activated Src. Using a CD44v5 alternative splicing reporter construct, we observed 99% inclusion of the alternatively spliced exon 5 following kep1 transfection in a cell line that constitutively expresses activated Src. This modulation in splicing was not observed in the parental NIH 3T3 cell line in which we obtained 7.5% exon 5 inclusion following kep1 transfection. Our data suggest a mechanism of action in which the in vivo phosphorylation status of the Kep1 protein affects its affinity towards its protein binding partners and in turn may allow for the modulation of alternative splice site selection in Kep1–ASF/SF2-dependent target genes.

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