Structural highlights
Disease
SIN3B_HUMAN SIN3A-related intellectual disability syndrome due to a point mutation.
Function
SIN3B_HUMAN Acts as a transcriptional repressor. Interacts with MXI1 to repress MYC responsive genes and antagonize MYC oncogenic activities. Interacts with MAD-MAX heterodimers by binding to MAD. The heterodimer then represses transcription by tethering SIN3B to DNA. Also forms a complex with FOXK1 which represses transcription. With FOXK1, regulates cell cycle progression probably by repressing cell cycle inhibitor genes expression.[UniProtKB:Q62141]
