SCUBA

PNRC2 — Proline rich nuclear receptor coactivator 2

PNRC2 belongs to a gene co-expression module in 4 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.

PNRC2's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsRNA Surveillance/NMD
RNA processing & translation
AFG3L2, ANKRD13A, ARPP19, BRD10, C5orf24, DNM1L, ERVK3-1, KCTD20 +8 more
Innate lymphoid cellsRNA Chromatin Regulation
RNA processing & translation
BTBD7, CCDC59, CWC25, DDX3Y, DNTTIP2, HNRNPU, KRR1, MRFAP1 +5 moreView in SCUBA
MacrophagesRNA Processing Housekeeping
Housekeeping
CISD3, CNIH4, DDX52, DPH3, EXOSC6, FABP5, GTF2E2, IKBKE +20 moreView in SCUBA
Smooth muscle cellsMuscle Energy Metabolism
Mitochondrial & OxPhos
ANP32B, HACD1, HEY2, MAP3K20, MRPS6, PIP5K1B, PPP1R1A, PRPSAP1 +4 moreView in SCUBA

About the gene

Chromosome1: 23956839-23963462
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Molecular functionActivator
Biological processNonsense-mediated mRNA decay, Transcription, Transcription regulation

Function

Involved in nonsense-mediated mRNA decay (NMD) by acting as a bridge between the mRNA decapping complex and the NMD machinery. May act by targeting the NMD machinery to the P-body and recruiting the decapping machinery to aberrant mRNAs. Required for UPF1/RENT1 localization to the P-body. Plays a role in glucocorticoid receptor-mediated mRNA degradation by interacting with the glucocorticoid receptor NR3C1 in a ligand-dependent manner when it is bound to the 5' UTR of target mRNAs and recruiting the RNA helicase UPF1 and the mRNA-decapping enzyme DCP1A, leading to RNA decay. Also acts as a nuclear receptor coactivator. May play a role in controlling the energy balance between energy storage and energy expenditure (By similarity).

Human Protein Atlas · Open Targets · UniProt

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