Mutant TP53 hijacks RNA-splicing factor RBM28 to suppress double-stranded RNA triggered antitumor immunity.

Abstract excerpt

TP53 mutation may not only compromise its multifaceted tumor-suppressive functions but also confer oncogenic properties. Here, we demonstrate that DNA-binding domain mutations of TP53 unexpectedly confer a transcriptional regulatory function, directly driving RNA-splicing factor RBM28 overexpression. Overexpressed RBM28 excessively splices transposon elements, inhibiting double-stranded RNA (dsRNA) formation,...

Topics

• Animals
• Tumor Suppressor Protein p53
• RNA-Binding Proteins
• Humans
• RNA, Double-Stranded
• Mice