SCUBA

DAZAP2 — DAZ associated protein 2

DAZAP2 belongs to a gene co-expression module in 5 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.

DAZAP2's module in each cell type

Cell typeModuleShares the module with
Innate lymphoid cellsInterferon-Stimulated Genes
Inflammation
ALDOA, CRTAP, DDX39B, EIF4B, GDI1, GNB2, GRINA, GSTM2 +17 moreView in SCUBA
MacrophagesAutophagy Vesicular Trafficking
Vesicular traficking
ACTR2, AHCYL1, ALKBH5, BECN1, BICD2, CAP1, CAPRIN1, COLGALT1 +32 moreView in SCUBA
Mucosal-associated invariant T cellHousekeeping Translation
Housekeeping
ARHGDIA, ARHGEF1, CCNI, EEF2, HLA-A, HLA-B, HNRNPA1, PABPC1 +4 more
Natural Killer cellsNK Cytotoxic Signaling
Cytotoxicity
BCL2L11, CBLB, CRYBG1, FYN, GPATCH8, HNRNPUL1, MAPK1, RAPGEF1 +3 moreView in SCUBA
PericytesTGF-beta Negative Feedback
Inflammatory
CTNND1, EMP1, KAT6A, KBTBD2, KLF7, MLKL, RCAN1, RGS3 +6 moreView in SCUBA

About the gene

SynonymsKIAA0058
Chromosome12: 51238724-51271362
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins

Function

In unstressed cells, promotes SIAH1-mediated polyubiquitination and degradation of the serine/threonine-protein kinase HIPK2, probably by acting as a loading factor that potentiates complex formation between HIPK2 and ubiquitin ligase SIAH1. In response to DNA damage, localizes to the nucleus following phosphorylation by HIPK2 and modulates the expression of a subset of TP53/p53 target genes by binding to TP53 at target gene promoters. This limits the expression of a number of cell death-mediating TP53 target genes, reducing DNA damage-induced cell death. Enhances the binding of transcription factor TCF7L2/TCF4, a Wnt signaling pathway effector, to the promoters of target genes (By similarity). Plays a role in stress granule formation.

Human Protein Atlas · Open Targets · UniProt

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