May serve as a nuclear matrix platform that organizes and integrates transcriptional responses. In osteoblasts, supports transcription activation: synergizes with RUNX2 to enhance FGFR2-mediated activation of the osteocalcin FGF-responsive element (OCFRE) (By similarity). Has also been shown to be an essential corepressor protein, which probably regulates different key pathways such as the Notch pathway. Negative regulator of the Notch pathway via its interaction with RBPSUH, which prevents the association between NOTCH1 and RBPSUH, and therefore suppresses the transactivation activity of Notch signaling. Blocks the differentiation of precursor B-cells into marginal zone B-cells. Probably represses transcription via the recruitment of large complexes containing histone deacetylase proteins. May bind both to DNA and RNA. Interacts with MSX2 and HIPK3 (By similarity). Interacts with NCOR2, HDAC1, HDAC2, RBBP4, MBD3 and MTA1L1. Interacts with RBPSUH; this interaction may prevent the interaction between RBPSUH and NOTCH1. Interacts with the nuclear receptors RAR and PPARD. Interacts with RAR in absence of ligand. Binds to the steroid receptor RNA coactivator SRA. (Microbial infection) Interacts with Epstein-Barr virus BSFL2/BMLF1. Associates with chromatin. Expressed at high level in brain, testis, spleen and thymus. Expressed at intermediate level in kidney, liver, mammary gland and skin. By 17-beta-estradiol. The RID domain mediates the interaction with nuclear receptors. The SPOC domain, which mediates the interaction with NCOR2, is essential for the repressive activity. The disease is caused by variants affecting the gene represented in this entry. Belongs to the RRM Spen family. Truncated N-terminus. Truncated N-terminus. Truncated N-terminus.