RNA-binding protein that acts as a mRNA splicing cofactor by promoting efficient splicing of transcripts that possess weak splice sites. Specifically promotes splicing of many cell-cycle and DNA-repair transcripts that possess weak splice sites, such as TUBG1, KATNB1, TUBGCP2, AURKB, PCNT, AKT1, RAD23A, and FANCG. Probably acts by facilitating the interaction between Serine/arginine-rich proteins such as SRSF2 and the RNA polymerase II. Also binds to DNA; binds to the consensus DNA sequence: 5'-GA[GT]AN[CG][AG]CC-3'. May indirectly repress hepatitis B virus (HBV) core promoter activity and transcription of HBV genes and production of HBV virions. Essential for correct RNA splicing of multiple genes critical for brain development, neuronal migration and metabolism, including TUBG1, FLNA, PNKP, WDR62, PSMD3, PCK2, PFKL, IDH2, and ACY1 (PubMed:27545680). Interacts with SRSF2. Associates with the spliceosome. Interacts with the AML1-MTG8 (AML1-ETO) fusion protein, possibly leading to trigger signals inhibiting leukemogenesis. Interacts with USH1G (PubMed:34023904). Colocalizes with the pre-mRNA splicing factor SRSF2. Experimental confirmation may be lacking for some isoforms. Widely expressed, with the higher expression seen in leukocyte and heart. Contains 8 types of repeats which are distributed in 3 regions. The disease is caused by variants affecting the gene represented in this entry. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. Contaminating sequence. Potential poly-A sequence. Extended N-terminus. Contaminating sequence. Sequence of unknown origin in the N-terminal part.