IndraLab
Statements
reach
"Mechanistically, loss of function mutations in zebrafishPRPF8 have been shown to result in missplicing of TP53, 36 while PRPF8 knockdown in mammalian cells led to increased compensatory transcriptional activity of TP53, 39 suggesting another possibility of synergetic interaction between PRPF8 defects and TP53."