PRDM1

This gene encodes a protein that acts as a repressor of beta-interferon gene expression. The protein binds specifically to the PRDI (positive regulatory domain I element) of the beta-IFN gene promoter. Transcription of this gene increases upon virus induction. Two alternatively spliced transcript variants that encode different isoforms have been reported.

PRDM1

Transcription factor that mediates a transcriptional program in various innate and adaptive immune tissue-resident lymphocyte T cell types such as tissue-resident memory T (Trm), natural killer (trNK) and natural killer T (NKT) cells and negatively regulates gene expression of proteins that promote the egress of tissue-resident T-cell populations from non-lymphoid organs. Plays a role in the development, retention and long-term establishment of adaptive and innate tissue-resident lymphocyte T cell types in non-lymphoid organs, such as the skin and gut, but also in other nonbarrier tissues like liver and kidney, and therefore may provide immediate immunological protection against reactivating infections or viral reinfection (By similarity).
Binds specifically to the PRDI element in the promoter of the beta-interferon gene (PubMed:1851123).
Drives the maturation of B-lymphocytes into Ig secreting cells (PubMed:12626569).
Associates with the transcriptional repressor ZNF683 to chromatin at gene promoter regions (By similarity).

Adaptive immune responseIEA:UniProtKB-KW
Aorta developmentIEA:Ensembl
Artery morphogenesisIEA:Ensembl
Cell fate commitmentManual Assertion Based On ExperimentIBA:GO_Central
Coronary vasculature developmentIEA:Ensembl
Eye photoreceptor cell developmentIEA:Ensembl
Gene expressionIEA:Ensembl
Germ cell developmentIEA:Ensembl
Heart valve developmentIEA:Ensembl
Histone arginine methylationIEA:Ensembl
Innate immune responseIEA:UniProtKB-KW
Intestinal epithelial cell developmentIEA:Ensembl
Kidney developmentIEA:Ensembl
Maternal placenta developmentIEA:Ensembl
Morphogenesis of a branching structureIEA:Ensembl
Negative regulation of gene expressionIEA:Ensembl
Negative regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIDA:NTNU_SB
Positive regulation of gene expressionIEA:Ensembl
Post-embryonic developmentIEA:Ensembl
Regulation of cell population proliferationIEA:Ensembl
Regulation of extrathymic T cell differentiationISS:UniProtKB
Regulation of gene expressionManual Assertion Based On ExperimentIBA:GO_Central
Regulation of natural killer cell differentiationISS:UniProtKB
Regulation of NK T cell differentiationISS:UniProtKB
Regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Response to radiationIEA:Ensembl
Sebum secreting cell proliferationIEA:Ensembl
Trophoblast giant cell differentiationIEA:Ensembl
Ventricular septum developmentIEA:Ensembl

Nucleus
Cytoplasm

In certain aggressive cases of activated B cell-like diffuse large B-cell lymphoma (ABC-DLBCL), PRDM1 protein instability has been observed. This instability, which impairs B-cell differentiation, is caused by N-terminal misfolding mutations, including those occurring at positions Pro-84 and Ile-107, and results in PRDM1 protein sequestration in the cytoplasm, followed by proteasomal degradation via a heat shock protein 70 HSPA1A-SYNV1/HRD1 pathway. These N-terminal mutations do not affect PRDM1 transcription regulation activity. HSPA1A inhibition restores PRDM1 nuclear localization and transcriptional activity in lymphoma cell lines and suppresses tumor growth in xenografts, more efficiently than proteasome inhibition.

Sumoylation at Lys-816 by PIAS1 augments transcriptional repressor activity, and is critical for plasma cell differentiation (PubMed:22555612).
Can be sumoylated with SUMO1 and SUMO2 by PML. Degradation of the wild-type protein mostly depends upon sumoylation, rather than ubiquitination (PubMed:28842558).
Desumoylated by SENP1 and SENP6 (PubMed:28842558).
Ubiquitinated by the SCF(FBXO11) complex, leading to its degradation by the proteasome.