a transcriptional repressor that binds specifically to the PRDI element in the promoter of the beta-interferon gene and can inhibit virus-mediated IFN-¿ production. Recruits chromatin-modifying enzymes including histone deacetylases and methyltransferases. Drives the maturation of B-lymphocytes into Ig secreting cells. Interacts with PRMT5. Expression of Blimp-1 is sufficient to drive terminal differentiation of BCL1 lymphoma cells into antibody secreting plasma cells, increasing the expression of the cell surface marker Syndecan-1. In the B-cell lineage, Blimp-1 is specifically expressed in antibody-secreting cells including activated B and plasma cells. In addition, Blimp-1 has been found during macrophage differentiation and in a subset of T-cells suggesting that it may play a wider role in homeostasis and differentiation. Target genes of Blimp-1 transcriptional repression with potential roles in differentiation include c-Myc, CIITA, Pax5, Spi-B, and Id3.Three isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Transcription, coactivator/corepressor; Transcription regulation; DNA binding protein; Methyltransferase, protein lysine, predicted; C2H2-type zinc finger protein
Cellular Component: cytoplasm; nucleus
Molecular Function: methyltransferase activity; protein binding; sequence-specific DNA binding; histone deacetylase binding; metal ion binding; transcription factor activity
Biological Process: negative regulation of lipopolysaccharide-mediated signaling pathway; eye photoreceptor cell development; cell fate commitment; transcription, DNA-dependent; positive regulation of B cell differentiation; negative regulation of transcription from RNA polymerase II promoter; negative regulation of B cell proliferation; maternal placenta development; germ cell development
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.