SCUBA

UNG — Uracil DNA glycosylase

UNG 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.

UNG's module in each cell type

Cell typeModuleShares the module with
CD8⁺ T cellsMCM Helicase Loading
Cell cycle
CDC45, CDCA7, DCTPP1, E2F1, GINS2, HELLS, MCM2, MCM3 +5 moreView in SCUBA
Gamma-delta T cellsCell Cycle Entry
Cell cycle
CDK4, DCTPP1, FH, GGCT, GSS, ISOC2, MBD3, MTHFD1 +4 more
Hematopoietic progenitor cellsDNA Replication S-phase
Cell cycle
CDT1, CENPH, CENPK, CHEK1, E2F1, FEN1, GINS2, GMNN +4 more
Mucosal-associated invariant T cellInnate Stress Activation
Stress
BATF, BCL2L1, BRD8, DNAJA3, FAM13A, IL6ST, LRRN3, OXNAD1 +5 more

About the gene

SynonymsDGU, HIGM4, UDG, UNG1, UNG2
Chromosome12: 109097597-109126725
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classDisease related genes, Enzymes, Human disease related genes, Potential drug targets, Predicted intracellular proteins, Predicted membrane proteins
Molecular functionHydrolase
Biological processDNA damage, DNA repair, Host-virus interaction

Function

Uracil-DNA glycosylase that hydrolyzes the N-glycosidic bond between uracil and deoxyribose in single- and double-stranded DNA (ssDNA and dsDNA) to release a free uracil residue and form an abasic (apurinic/apyrimidinic; AP) site. Excises uracil residues arising as a result of misincorporation of dUMP residues by DNA polymerase during replication or due to spontaneous or enzymatic deamination of cytosine. Mediates error-free base excision repair (BER) of uracil at replication forks. According to the model, it is recruited by PCNA to S-phase replication forks to remove misincorporated uracil at U:A base mispairs in nascent DNA strands. Via trimeric RPA it is recruited to ssDNA stretches ahead of the polymerase to allow detection and excision of deaminated cytosines prior to replication. The resultant AP sites temporarily stall replication, allowing time to repair the lesion. Mediates mutagenic uracil processing involved in antibody affinity maturation. Processes AICDA-induced U:G base mispairs at variable immunoglobulin (Ig) regions leading to the generation of transversion mutations. Operates at switch sites of Ig constant regions where it mediates Ig isotype class switch recombination. Excises AICDA-induced uracil residues forming AP sites that are subsequently nicked by APEX1 endonuclease. The accumulation of staggered nicks in opposite strands results in double strand DNA breaks that are finally resolved via non-homologous end joining repair pathway (By similarity).

Human Protein Atlas · Open Targets · UniProt

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