SCUBA

PRMT2 — Protein arginine methyltransferase 2

PRMT2 belongs to a gene co-expression module in 6 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.

PRMT2's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsGIMAP survival
Immune regulation
ABLIM1, AKT3, ANKRD13D, ARL4C, C16orf54, CA5B, COPA, CRBN +16 moreView in SCUBA
Gamma-delta T cellsTCR Proximal Signaling
TCR Signaling
ADGRG5, BIN2, C11orf21, C12orf75, CD300A, FGR, GPSM3, LAT +11 more
Innate lymphoid cellsNK Cytotoxic Regulation
Cytotoxicity
ARHGAP30, BIN2, CAPN12, CHD9, CLK1, CTSC, CYB5B, DDX27 +29 moreView in SCUBA
Mucosal-associated invariant T cellChromatin Epigenetic Regulation
DNA/chromatin regulation
ACAP2, APBB1IP, ARHGAP25, ATM, CD247, CHD9, CLCN3, DDX17 +14 more
Natural Killer cellsNK Homing & Residency
Homing & TEM
C11orf21, CD47, CTSW, FXYD5, RIPOR2, S1PR4, SAMHD1, TFDP2 +2 moreView in SCUBA
Smooth muscle cellsLysosomal-secretory processing
Protein processing & ER
BZW2, COPZ1, CTSL, LAMP1, PIGT, PLOD2, RGS9, RPN2 +5 moreView in SCUBA

About the gene

SynonymsHRMT1L1, MGC111373
Chromosome21: 46635595-46665124
Predicted locationIntracellular
Essential geneNo
Protein classEnzymes, Predicted intracellular proteins
Molecular functionMethyltransferase, Transferase

Function

Arginine methyltransferase that methylates the guanidino nitrogens of arginyl residues in proteins such as STAT3, FBL, histone H4. Acts as a coactivator (with NCOA2) of the androgen receptor (AR)- mediated transactivation. Acts as a coactivator (with estrogen) of estrogen receptor (ER)-mediated transactivation. Enhances PGR, PPARG, RARA-mediated transactivation. May inhibit NF-kappa-B transcription and promote apoptosis. Represses E2F1 transcriptional activity (in a RB1- dependent manner). May be involved in growth regulation.

Human Protein Atlas · Open Targets · UniProt

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