NAA25: N-alpha-acetyltransferase 25, NatB auxiliary subunit
A core component of the NatB N-terminal acetyltransferase complex involved in protein stability and cell cycle regulation
Gene Information Card
| Symbol | NAA25 |
|---|---|
| Full Name | N-alpha-acetyltransferase 25, NatB auxiliary subunit |
| Gene Type | protein-coding |
| Chromosomal Location | 12q24.31 |
| NCBI Gene ID | 80018 ncbi.nlm.nih.gov/gene/80018 |
| Ensembl ID | ENSG00000111224 |
| UniProt ID | Q9BQQ3 |
| OMIM ID | 612770 |
| HGNC ID | 24018 |
| Aliases | MDM20, NATH, C12orf30 |
Description
NAA25 encodes the auxiliary subunit of the NatB N-terminal acetyltransferase complex, which catalyzes the cotranslational acetylation of proteins with N-terminal methionine followed by acidic or asparagine residues. This modification influences protein stability, localization, and interactions. NAA25 is essential for cell cycle progression and has been implicated in tumorigenesis and neurodevelopmental disorders.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Breast cancer | NAA25 overexpression promotes cell proliferation and migration via altered acetylation of oncogenic substrates | PMID: 25605274 |
| Colorectal cancer | NAA25 amplification correlates with poor prognosis and increased tumor growth | PMID: 27197152 |
| Neurodevelopmental disorder | Homozygous loss-of-function mutations in NAA25 cause intellectual disability and microcephaly | PMID: 31006510 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Testis | 12.3 | Medium |
| Brain | 8.7 | Medium |
| Liver | 6.2 | Low |
| Heart | 5.1 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HEK293 | 10.5 | High expression |
| HeLa | 8.9 | Moderate expression |
| MCF7 | 7.3 | Moderate expression |
| HepG2 | 5.8 | Low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1A>G (p.Met1?) | Missense | <0.01% | Loss of start codon, likely loss of function |
| c.742C>T (p.Arg248*) | Nonsense | <0.01% | Premature truncation, loss of function |
| c.1234G>A (p.Glu412Lys) | Missense | 0.02% | Unknown functional effect |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations in NAA25 lead to truncated protein and loss of NatB complex activity, associated with neurodevelopmental phenotypes.
Gain of Function (GOF)
Amplification and overexpression of NAA25 in cancers may enhance NatB activity, promoting oncogenic signaling.
Dominant Negative (DN)
No dominant-negative mutations have been reported for NAA25.
View complete mutation data：
Gene Ontology (GO)
| • peptide alpha-N-acetyltransferase activity (GO:0004596) | • cytoplasm (GO:0005737) |
| • cytosol (GO:0005829) | • nucleus (GO:0005634) |
| • cellular protein modification process (GO:0006464) | • cell cycle (GO:0007049) |
Pathways
• N-terminal acetylation (NatB complex)
• Cell cycle regulation
Protein Summary
NAA25 is a 866-amino acid protein that serves as the auxiliary subunit of the NatB N-terminal acetyltransferase complex. It binds to the catalytic subunit NAA20 and is required for complex stability and substrate recognition. The protein is widely expressed, with highest levels in testis and brain. NAA25 contains WD40 repeats that mediate protein-protein interactions. Its dysregulation contributes to cancer progression and neurodevelopmental disorders.
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