Fig 1: Artificial antisense oligonucleotides (ASOs) designed to induce GTF2H4 alternative splicing facilitate p52 C-terminal truncation and promote TFIIH stability.(A) Schematic representation of the GTF2H4 gene structure and the design of ASOs to induce intron 13 inclusion, leading to a frameshift and a C-terminal truncation of p52. In-frame stop codons in intron 13 (orange). (B) Induction of p52 C-terminal truncation in TTD-A cells treated with ASOs (24 hours). (C and D) Simultaneous blocking of the 5’ and 3’ splice sites of intron 13 facilitates efficient induction of the p52 truncation and TFIIH stabilization in TTD-A cells. In D, immunoprecipitation of XPB/p89 was performed. Asterisks indicate nonspecific products. (E) ASO treatment mostly rescues transcription in TTD cells. Transcription activity was measured by EU incorporation. Bars and error bars represent means and SEM, respectively, of experiments (n = 3, as indicated by the colored-circles and their corresponding plots). 20J/m2 UVC-irradiation. wo, without treatment; control, control-ASO treatment.