PTBP1 and posterior cortical atrophy: detected that DNMT3B knockdown efficiently sensitized PCa cells to irradiation.[31] Actually, more than 40 splice variants were identified for DNMT3B, but their functions and regulation remain largely unclear.[32] Our data demonstrated that PTBP1 obviously repressed exon 5 skipping that compromises the expression of the truncated splicing variant DNMT3B through binding to the motif in the intron 5.