SCUBA

PIAS2 — Protein inhibitor of activated STAT 2

PIAS2 belongs to a gene co-expression module in 2 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

PIAS2's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsTCR-Cytokine Signaling
TCR Signaling
ARHGAP26, CACNA2D2, CCDC88C, LPGAT1, LY75, MED15, NBPF14, NBPF19 +10 more
MacrophagesMITF Lysosomal Program
Lysosomal & pahgocytosis
ABHD3, ANKRD44, ARSB, C2CD5, CERS6, CHST11, CNST, DCTN4 +25 moreView in SCUBA

About the gene

SynonymsARIP3, miz, PIASX-ALPHA, PIASX-BETA, ZMIZ4
Chromosome18: 46803218-46920160
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classPredicted intracellular proteins, Predicted membrane proteins
Molecular functionDNA-binding, Transferase
Biological processTranscription, Transcription regulation, Ubl conjugation pathway

Function

Functions as an E3-type small ubiquitin-like modifier (SUMO) ligase, stabilizing the interaction between UBE2I and the substrate, and as a SUMO-tethering factor. Plays a crucial role as a transcriptional coregulator in various cellular pathways, including the STAT pathway, the p53 pathway and the steroid hormone signaling pathway. The effects of this transcriptional coregulation, transactivation or silencing may vary depending upon the biological context and the PIAS2 isoform studied. However, it seems to be mostly involved in gene silencing. Binds to sumoylated ELK1 and enhances its transcriptional activity by preventing recruitment of HDAC2 by ELK1, thus reversing SUMO-mediated repression of ELK1 transactivation activity. Isoform PIAS2-beta, but not isoform PIAS2-alpha, promotes MDM2 sumoylation. Isoform PIAS2-alpha promotes PARK7 sumoylation. Isoform PIAS2-beta promotes NCOA2 sumoylation more efficiently than isoform PIAS2-alpha. Isoform PIAS2-alpha sumoylates PML at'Lys-65' and 'Lys-160'.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.