Affinage

NAA10

N-alpha-acetyltransferase 10 · UniProt P41227

Length
235 aa
Mass
26.5 kDa
Annotated
2026-06-10
58 papers in source corpus 28 papers cited in narrative 28 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NAA10 is the catalytic subunit of the NatA N-terminal acetyltransferase complex, which it forms with the auxiliary subunit NAA15 to co-translationally acetylate the N-termini of NatA-class substrates (PMID:24408909, PMID:25099252). Its N-terminal acetyltransferase activity and substrate specificity are conserved from zebrafish to human, and loss of function produces essential developmental phenotypes including growth retardation and axis/eye defects (PMID:26251455). NAA10 catalytic activity exists in two functionally separable forms — monomeric NAA10 NAT activity and NAA15-dependent NatA complex activity — and disease-associated missense variants impair these through distinct biochemical mechanisms: reduced monomeric catalysis, impaired NatA complex assembly, or decreased protein stability (PMID:29748569, PMID:29558889, PMID:32698785, PMID:33255974, PMID:35039925). The severity of NAA10-related (Ogden) syndrome tracks with the degree to which a given substitution disrupts NatA complex formation and residual catalytic activity (PMID:24408909, PMID:25099252, PMID:41973310). In mice, the loss of Naa10 is genetically buffered by the paralog Naa12, which retains NAT activity, such that single Naa10 knockout shows no global acetylation defect whereas Naa10/Naa12 double knockout is embryonic lethal (PMID:34355692). Beyond its catalytic role, NAA10 is stabilized and activated by neddylation at K148 via the RBX1-CUL4A/UBE2M machinery (PMID:41857595), and NatA-dependent activity feeds into developmental signaling, modulating FGF/MAPK output and epiblast specification (PMID:30993557) and retinoic-acid pathway gene expression (PMID:24431331). Whether NAA10 acts as a genuine lysine (internal) acetyltransferase is contested: recombinant NAA10 failed to acetylate proposed lysine substrates above background (PMID:26755727), and Trp38 hydroxylation by FIH proposed to switch NAA10 to a KAT was not detectable in human cells (PMID:34769235).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2014 High

    Established NAA10 as the catalytic subunit of NatA and showed that the Ogden syndrome S37P substitution causes disease by reducing both catalysis and NAA15 complexation, defining a loss-of-function mechanism.

    Evidence Yeast complementation, immunoprecipitation, in vitro NAT assay, and quantitative Nt-acetylome proteomics; parallel in vitro NAT assays across variants

    PMID:24408909 PMID:25099252

    Open questions at the time
    • Did not separate monomeric NAA10 dysfunction from NatA complex dysfunction
    • Substrate-level consequences in human cells not mapped
  2. 2014 Medium

    Linked NAA10 loss to a defined human cellular phenotype, showing protein loss disrupts proliferation and dysregulates retinoic-acid pathway gene expression.

    Evidence Patient fibroblasts with splice-donor mutation; Western blot, proliferation, retinol uptake, and expression arrays

    PMID:24431331

    Open questions at the time
    • Direct acetylation substrates linking NAA10 to retinoic-acid genes not identified
    • Causality vs. correlation of transcriptional changes unresolved
  3. 2015 Medium

    Demonstrated conservation of NAA10 NAT activity and substrate specificity and an essential developmental requirement in a vertebrate model.

    Evidence In vitro NAT assay of zebrafish Naa10; morpholino knockdown with developmental phenotyping

    PMID:26251455

    Open questions at the time
    • Morpholino off-target effects not fully excluded
    • Specific substrates underlying developmental phenotypes unknown
  4. 2016 High

    Challenged the proposed lysine-acetyltransferase function by showing recombinant NAA10 does not acetylate reported KAT substrates above background.

    Evidence In vitro reconstitution acetylation assays with purified recombinant proteins across multiple substrates (MSRA, MLCK, RUNX2)

    PMID:26755727

    Open questions at the time
    • Cannot exclude KAT activity requiring cofactors or partners absent in vitro
    • Does not address context-specific KAT activity in cells
  5. 2018 Medium

    Resolved that monomeric NAA10 catalysis and NatA complex catalysis are functionally separable, with variants able to impair one while sparing the other.

    Evidence In vitro NAT assays of monomeric vs. NatA complex plus cycloheximide chase for p.I72T and p.V111G

    PMID:29558889 PMID:29748569

    Open questions at the time
    • Physiological role of monomeric NAA10 activity distinct from NatA not defined
    • In vivo substrates of monomeric form unknown
  6. 2019 Medium

    Showed HYPK modulates reconstituted NatA enzymatic activity and that variants impair complex activity in a subunit-context-dependent manner.

    Evidence In vitro NAT assays with reconstituted NatA ±HYPK across variants; additional monomeric assays with Ac-CoA-binding structural modeling

    PMID:31127942 PMID:31174490

    Open questions at the time
    • HYPK regulatory mechanism at residue level not resolved
    • Cellular relevance of HYPK modulation not tested
  7. 2019 Medium

    Placed NAA10-mediated acetylation upstream of developmental signaling, showing Naa10 loss augments FGF/MAPK and biases lineage choice.

    Evidence Naa10 knockout mESC differentiation and pathway analysis

    PMID:30993557

    Open questions at the time
    • Direct NAA10 substrate in the FGF/MAPK axis not identified
    • Single cellular system
  8. 2020 Medium

    Defined distinct pathogenic mechanisms at the assembly level, with variants selectively disrupting NatA complex formation, monomeric catalysis, or stability, sometimes in opposing directions.

    Evidence Immunoprecipitation and in vitro NAT assays (monomeric and complex) plus cycloheximide chase for p.H16P, p.D10G, p.L11R

    PMID:32698785 PMID:33255974

    Open questions at the time
    • Genotype-phenotype correlation for opposing biochemical effects not clinically resolved
    • Single-lab biochemistry
  9. 2021 High

    Revealed genetic redundancy by identifying the paralog Naa12, explaining the mild single-knockout phenotype and establishing combined NAT activity as essential for viability.

    Evidence Mouse single and double knockout genetics with enzymatic activity assays

    PMID:34355692

    Open questions at the time
    • Relative substrate division between Naa10 and Naa12 in vivo not mapped
    • Tissue-specific dependence unclear
  10. 2021 Medium

    Tested and rejected a proposed NAT-to-KAT regulatory switch, finding no NAA10 Trp38 hydroxylation or FIH interaction in human cells.

    Evidence Mass spectrometry, Co-IP, and cell fractionation across multiple human cell lines (negative result)

    PMID:34769235

    Open questions at the time
    • Cannot exclude transient or condition-specific hydroxylation
    • Does not resolve KAT activity question broadly
  11. 2026 Medium

    Identified neddylation at K148 by RBX1-CUL4A/UBE2M as a post-translational input that stabilizes and activates NAA10, integrating it into the neddylation signaling pathway.

    Evidence Co-IP, mass spectrometry, proximity ligation, K148 mutagenesis, and knockdown in prostate cancer cells and xenografts

    PMID:41857595

    Open questions at the time
    • Downstream NAA10 substrates mediating proliferation not identified
    • Generality beyond cancer context untested
  12. 2026 Medium

    Reopened the lysine-acetyltransferase model with mutagenesis-supported claims that NAA10 acetylates specific lysines on C7orf50 (nutrient/mTOR-responsive) and CREBRF, despite continued controversy over KAT activity.

    Evidence In vitro and in vivo acetylation assays with target-lysine mutagenesis, localization imaging, mTOR perturbation; separate Co-IP and ubiquitination/acetylation assays

    PMID:42139339 PMID:42262012

    Open questions at the time
    • Conflicts with prior negative reconstitution data (PMID 26755727)
    • Whether acetylation is direct or via an associated activity not fully excluded
    • Reproducibility across labs not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Whether NAA10 possesses bona fide internal lysine-acetyltransferase activity in vivo, and which physiological substrates it acetylates beyond NatA-type N-termini, remains unresolved.
  • No independently replicated, cofactor-defined demonstration of cellular KAT activity
  • Mechanistic basis for reconciling positive and negative KAT findings absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0140096 catalytic activity, acting on a protein 3
Localization
GO:0005730 nucleolus 1
Pathway
R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 2
Partners
C7ORF50CUL4AHYPKNAA12NAA15NME3RBX1UBE2M
Complex memberships
NatA complex

Evidence

Reading pass · 28 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 The Ogden syndrome NAA10 p.Ser37Pro (S37P) mutant shows reduced in vitro catalytic activity and reduced subunit complexation with NAA15 in immunoprecipitation experiments. In a yeast complementation model, wild-type human NatA fully rescued NatA-deletion yeast phenotypes whereas the S37P mutant only partially rescued, and quantitative Nt-acetylome analysis showed globally reduced N-terminal acetylation of NatA substrates in yeast expressing the mutant compared to wild-type hNatA. Yeast complementation (genetic epistasis), immunoprecipitation, in vitro N-terminal acetylation assay, quantitative Nt-acetylome proteomics Molecular & cellular proteomics : MCP High 24408909
2016 Recombinant Naa10/ARD1 does not acetylate lysine residues of reported substrates (MSRA, MLCK, RUNX2) above background levels in vitro, suggesting previously reported lysine acetylation events are chemical rather than enzymatic; no difference was detected with or without Naa10 in the reaction. In vitro reconstitution acetylation assay with recombinant proteins The Journal of biological chemistry High 26755727
2014 NAA10 is the catalytic subunit of the NatA complex (with auxiliary subunit NAA15); in vitro N-terminal acetylation assays showed that disease-associated missense variants (including p.Ser37Pro) have reduced catalytic activity, and phenotypic severity correlates with the degree of residual NatA catalytic activity. In vitro N-terminal acetylation assays European journal of human genetics : EJHG Medium 25099252
2015 Zebrafish Naa10 (zNaa10) possesses N-terminal acetyltransferase activity with substrate specificity highly similar to human NAA10, as demonstrated by in vitro NAT assays; morpholino-mediated knockdown of naa10 in zebrafish caused increased lethality, growth retardation, bent axis, abnormal eyes and bent tails, establishing an essential developmental role. In vitro N-terminal acetylation assay; morpholino knockdown in zebrafish with phenotypic readout Bioscience reports Medium 26251455
2015 The NAA10 p.Tyr43Ser mutant shows significantly decreased catalytic activity and reduced protein stability compared to wild-type in in vitro assays, demonstrating that the Tyr43 residue is important for both enzymatic activity and stability. In vitro N-terminal acetylation assay; protein stability assessment Scientific reports Medium 26522270
2016 In vitro enzymatic assays for NAA10 missense variants p.Arg83Cys and p.Phe128Leu revealed reduced catalytic N-terminal acetyltransferase activity, linking these variants to pathogenicity. In vitro N-terminal acetylation assay Human mutation Medium 27094817
2019 Biochemical analyses of NAA10 and NAA15 variants as part of the human NatA complex, including with and without the HYPK regulatory subunit, showed variant-specific impairment of N-terminal acetyltransferase activity, with HYPK modulating NatA enzymatic activity. In vitro N-terminal acetylation assay with reconstituted NatA complex ± HYPK Human molecular genetics Medium 31127942
2018 NAA10 p.Ile72Thr variant is protein-destabilized and has decreased monomeric NAT activity, but NatA complex activity (with NAA15) appears normal; binding to NAA15 is most likely intact, suggesting distinct roles for monomeric NAA10 vs. NatA complex activity. In vitro acetylation assay (monomeric and NatA complex); protein stability studies European journal of human genetics : EJHG Medium 29748569
2018 NAA10 p.V111G has reduced monomeric catalytic activity and reduced protein stability, but NatA complex activity is unaltered, as shown by cycloheximide chase and in vitro acetylation assays; this represents isolated monomeric NAA10 dysfunction without NatA impairment. In vitro N-terminal acetylation assay (monomeric vs. NatA complex); cycloheximide chase BMC medical genetics Medium 29558889
2019 NAA10 p.R83H has reduced monomeric catalytic acetyltransferase activity, likely due to impaired enzyme-Ac-CoA binding, as modeled by the altered charge density in the Ac-CoA binding region; NatA complex activity was not separately assessed. In vitro N-terminal acetylation assay (monomeric NAA10); structural modeling BMC medical genetics Low 31174490
2020 NAA10 p.His16Pro impairs NatA complex formation and NatA catalytic activity, while monomeric NAA10 catalytic activity and cellular protein stability are unaffected, as shown by immunoprecipitation and in vitro acetylation assays; cycloheximide chase confirmed normal stability. Immunoprecipitation (NatA complex formation); in vitro N-terminal acetylation assay; cycloheximide chase BMC medical genetics Medium 32698785
2020 NAA10 p.D10G and p.L11R variants both impair complex formation with NAA15 (shown by immunoprecipitation), but have opposing effects on catalytic activity: D10G retains normal NatA activity but reduced monomeric NAT activity, while L11R shows reduced NatA activity but normal monomeric NAT activity. Immunoprecipitation; in vitro N-terminal acetylation assay (monomeric and NatA complex) International journal of molecular sciences Medium 33255974
2020 Monomeric recombinant hARD1/NAA10 exhibits lysine acetyltransferase (KAT) activity in vitro, but this activity is lost as the protein forms oligomers over time; size-exclusion analysis showed oligomeric NAA10 lacks KAT activity while the monomeric form retains it, with activity dependent on reactant concentrations and reaction time. In vitro lysine acetylation assay; size-exclusion chromatography Molecules (Basel, Switzerland) Low 32013195
2021 NAA10 Trp38 hydroxylation by FIH (factor inhibiting HIF-1α) could not be detected in multiple human cell lines, and no interaction between NAA10 and FIH was found, indicating that Trp38 hydroxylation is not a regulatory switch converting NAA10 from NAT to KAT activity in human cells. Mass spectrometry (hydroxylation detection); Co-IP (NAA10-FIH interaction); cell fractionation in multiple human cell lines International journal of molecular sciences Medium 34769235
2021 Naa12, a previously unannotated Naa10 paralog with NAT activity, genetically compensates for Naa10 in mice; Naa10 single-knockout male mice do not show globally apparent amino-terminal acetylation impairment, but Naa10/Naa12 double-knockout mice are embryonic lethal, establishing Naa12 as a functional redundant enzyme. Mouse knockout genetics (single and double knockout); phenotypic analysis; enzymatic activity assays eLife High 34355692
2022 Biochemical characterization of novel NAA10 variants (p.A6P, p.R79C, p.Q129P, p.E157K) by in vitro acetylation assays revealed distinct impacts on N-terminal acetyltransferase activity, with some variants specifically impairing monomeric NAA10 activity while others impair NatA complex activity, suggesting multiple distinct pathogenic mechanisms. In vitro N-terminal acetylation assay (monomeric and NatA complex) Human genetics Medium 35039925
2019 Naa10 deficiency in mouse embryonic stem cells augments FGF/MAPK signaling and attenuates differentiation towards the epiblast lineage (deviating towards primitive endoderm), demonstrating a role for Naa10-mediated N-terminal acetylation in regulating FGF/MAPK pathway activity and epiblast specification. Naa10 knockout mESCs; differentiation assays; pathway analysis In vitro cellular & developmental biology. Animal Medium 30993557
2018 siRNA screen identified NAA10 as a factor in the transcriptional machinery regulating PXR (pregnane X receptor) transcription in pancreatic cancer cells; NAA10 knockdown reduced PXR transcript levels. siRNA library screen; deconvolution validation; qRT-PCR Biochemical pharmacology Low 30566892
2016 Stable knockdown of Naa10 in H1299 cells caused morphological changes and, by cDNA microarray, upregulation of netrin-1 (NTN1) and its receptor UNC5B as early downstream targets; this relationship was validated in mouse embryos and upon all-trans retinoic acid treatment, indicating Naa10 negatively regulates NTN1/UNC5B expression. Stable shRNA knockdown; cDNA microarray; validation in mouse embryo tissue; retinoic acid treatment Scientific reports Low 27910960
2024 RGMB-AS1 lncRNA binds to the 82–87 amino acid region of NAA10, stimulating its acetyltransferase activity and promoting the conversion of acetyl-CoA to HMG-CoA, contributing to ferroptosis in NSCLC; this was demonstrated by co-IP and functional assays. Co-immunoprecipitation; in vitro acetyltransferase activity assay; cell and xenograft functional assays Cancer letters Low 38574881
2026 NAA10 promotes acetylation of CREBRF, which facilitates BTRC (an E3 ubiquitin ligase)-mediated ubiquitination and degradation of CREBRF, thereby activating endoplasmic reticulum stress and exacerbating renal tubular injury in diabetic kidney disease; interactions confirmed by Co-IP. Co-immunoprecipitation; ubiquitination/acetylation assays; knockdown/overexpression in HK-2 cells and STZ mouse model Journal of diabetes investigation Low 42262012
2026 UBE2M promotes neddylation of NAA10 at K148, mediated by the RBX1-CUL4A E3 ligase complex, which enhances NAA10 protein stability and functional activity; knockdown of NAA10 suppressed UBE2M-driven prostate cancer cell proliferation, placing NAA10 downstream of the UBE2M neddylation pathway. Co-immunoprecipitation; mass spectrometry; proximity ligation assay; site-directed mutagenesis (K148); knockdown/overexpression in PCa cells and xenografts Journal of translational medicine Medium 41857595
2026 NAA10 acetylates C7orf50 at lysine-71/72/76 residues; this acetylation, regulated by mTOR (which phosphorylates NAA10 as a nutritional status-responsive acetyltransferase), determines C7orf50 nucleolar localization and coordinates ribosome biogenesis vs. autophagy in response to nutrient status. In vitro and in vivo acetylation assays; site-directed mutagenesis; localization imaging; mTOR pathway perturbation Science advances Medium 42139339
2026 NME3 interacts with NAA10 in human dental pulp stem cells (identified by mass spectrometry and confirmed by colocalization); NAA10 knockdown rescued odontogenic differentiation deficits caused by NME3 silencing, and NAA10 overexpression attenuated NME3 effects, placing NAA10 as a downstream effector of NME3 in regulating RUNX2 nuclear translocation. Mass spectrometry; colocalization imaging; knockdown rescue assay; overexpression assay FASEB journal Low 42165278
2024 Computational structural analysis of NAA10 F128I and F128L disease-associated mutations revealed that F128I reduces flexibility of the substrate-binding region (impairing substrate peptide binding), while F128L reduces flexibility of the Ac-CoA binding region, demonstrating two mechanistically distinct paths to catalytic inactivation. Molecular dynamics simulation; structural modeling; conformational plasticity analysis Computational and structural biotechnology journal Low 39610905
2014 Patient fibroblasts from males with the NAA10 c.471+2T→A splice donor mutation lacked full-length NAA10 protein and showed cell proliferation defects; retinol uptake was decreased in patient cells, and expression arrays showed significant dysregulation of genes in the retinoic acid signalling pathway including BMP4, STRA6, and downstream targets of BCOR and canonical WNT. Protein expression (Western blot); cell proliferation assay; retinol uptake assay; expression array Journal of medical genetics Medium 24431331
2021 Down-regulation of NAA10 in rat OGD/R and MCAO models reversed the attenuation of ERK1/2 phosphorylation normally induced by sevoflurane preconditioning, indicating NAA10 mediates neuroprotective effects through regulation of ERK1/2 phosphorylation. siRNA knockdown in vitro (OGD/R) and in vivo (MCAO); Western blot for phospho-ERK1/2; TTC staining; TUNEL assay Neuroscience letters Low 33872734
2026 In a NAA10 knockout (ΔNAA10) glioblastoma cell line generated by CRISPR/Cas9, patient variants p.L126R and p.F128L severely impaired NatA complex formation and altered cellular distribution of NAA10, while p.L126V maintained near-wild-type protein stability and colocalization with NAA15, demonstrating that clinical severity is driven by the specific amino acid substitution's effect on NatA complex assembly. CRISPR/Cas9 NAA10 knockout cell line; GFP-tagged variant re-expression; colocalization imaging with NAA15 Molecular and cellular pediatrics Medium 41973310

Source papers

Stage 0 corpus · 58 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 A splice donor mutation in NAA10 results in the dysregulation of the retinoic acid signalling pathway and causes Lenz microphthalmia syndrome. Journal of medical genetics 88 24431331
2015 The biological functions of Naa10 - From amino-terminal acetylation to human disease. Gene 84 25987439
2016 Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency. Human mutation 78 27094817
2014 De novo missense mutations in the NAA10 gene cause severe non-syndromic developmental delay in males and females. European journal of human genetics : EJHG 78 25099252
2015 NAA10 mutation causing a novel intellectual disability syndrome with Long QT due to N-terminal acetyltransferase impairment. Scientific reports 71 26522270
2016 microRNA-342-5p and miR-608 inhibit colon cancer tumorigenesis by targeting NAA10. Oncotarget 62 26646451
2019 Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15. Human molecular genetics 59 31127942
2018 NAA10-related syndrome. Experimental & molecular medicine 52 30054457
2014 A Saccharomyces cerevisiae model reveals in vivo functional impairment of the Ogden syndrome N-terminal acetyltransferase NAA10 Ser37Pro mutant. Molecular & cellular proteomics : MCP 48 24408909
2015 The N-terminal acetyltransferase Naa10 is essential for zebrafish development. Bioscience reports 47 26251455
2023 Expanding the phenotypic spectrum of NAA10-related neurodevelopmental syndrome and NAA15-related neurodevelopmental syndrome. European journal of human genetics : EJHG 43 37130971
2016 The N-terminal Acetyltransferase Naa10/ARD1 Does Not Acetylate Lysine Residues. The Journal of biological chemistry 43 26755727
2024 LncRNA RGMB-AS1 inhibits HMOX1 ubiquitination and NAA10 activation to induce ferroptosis in non-small cell lung cancer. Cancer letters 41 38574881
2018 A novel NAA10 variant with impaired acetyltransferase activity causes developmental delay, intellectual disability, and hypertrophic cardiomyopathy. European journal of human genetics : EJHG 34 29748569
2018 NAA10 dysfunction with normal NatA-complex activity in a girl with non-syndromic ID and a de novo NAA10 p.(V111G) variant - a case report. BMC medical genetics 31 29558889
2018 ARD1/NAA10 acetylation in prostate cancer. Experimental & molecular medicine 30 30054487
2019 NAA10 polyadenylation signal variants cause syndromic microphthalmia. Journal of medical genetics 29 30842225
2022 Biochemical analysis of novel NAA10 variants suggests distinct pathogenic mechanisms involving impaired protein N-terminal acetylation. Human genetics 28 35039925
2017 Clinical Manifestations Associated With the N-Terminal-Acetyltransferase NAA10 Gene Mutation in a Girl: Ogden Syndrome. Pediatric neurology 28 28967461
2018 N-α-acetyltransferase 10 (NAA10) in development: the role of NAA10. Experimental & molecular medicine 25 30054454
2020 Severe syndromic ID and skewed X-inactivation in a girl with NAA10 dysfunction and a novel heterozygous de novo NAA10 p.(His16Pro) variant - a case report. BMC medical genetics 23 32698785
2018 ARD1/NAA10 in hepatocellular carcinoma: pathways and clinical implications. Experimental & molecular medicine 23 30054466
2019 A novel NAA10 p.(R83H) variant with impaired acetyltransferase activity identified in two boys with ID and microcephaly. BMC medical genetics 21 31174490
2021 Confirmation of Ogden syndrome as an X-linked recessive fatal disorder due to a recurrent NAA10 variant and review of the literature. American journal of medical genetics. Part A 18 34075687
2018 Versatility of ARD1/NAA10-mediated protein lysine acetylation. Experimental & molecular medicine 18 30054464
2021 Clinical Manifestations in a Girl with NAA10-Related Syndrome and Genotype-Phenotype Correlation in Females. Genes 15 34200686
2020 NAA10 promotes proliferation of renal cell carcinoma by upregulating UPK1B. European review for medical and pharmacological sciences 15 33275221
2020 NAA10 variant in 38-week-gestation male patient: a case study. Cold Spring Harbor molecular case studies 14 33335012
2023 NAA10 overexpression dictates distinct epigenetic, genetic, and clinicopathological characteristics in adult gliomas. Journal of neuropathology and experimental neurology 12 37253389
2021 Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway. eLife 12 34355692
2020 Characterization of Lysine Acetyltransferase Activity of Recombinant Human ARD1/NAA10. Molecules (Basel, Switzerland) 12 32013195
2024 Conformational plasticity links structural instability of NAA10F128I and NAA10F128L mutants to their catalytic deregulation. Computational and structural biotechnology journal 9 39610905
2020 A Japanese boy with NAA10-related syndrome and hypertrophic cardiomyopathy. Human genome variation 9 32864149
2018 RNA interference screen identifies NAA10 as a regulator of PXR transcription. Biochemical pharmacology 9 30566892
2016 Unc-5 homolog B (UNC5B) is one of the key downstream targets of N-α-Acetyltransferase 10 (Naa10). Scientific reports 9 27910960
2022 iTRAQ and two-dimensional-LC-MS/MS reveal NAA10 is a potential biomarker in esophageal squamous cell carcinoma. Proteomics. Clinical applications 7 35182098
2019 Ocular Manifestations of the NAA10-Related Syndrome. Case reports in genetics 7 31093388
2023 Phenotypic variability and gastrointestinal manifestations/interventions for growth in NAA10-related neurodevelopmental syndrome. American journal of medical genetics. Part A 6 36810866
2021 Down-regulation of NAA10 mediates the neuroprotection induced by sevoflurane preconditioning via regulating ERK1/2 phosphorylation. Neuroscience letters 5 33872734
2021 Hydroxylation of the Acetyltransferase NAA10 Trp38 Is Not an Enzyme-Switch in Human Cells. International journal of molecular sciences 4 34769235
2024 Evaluating possible maternal effect lethality and genetic background effects in Naa10 knockout mice. PloS one 3 38713657
2020 NAA10 p.(D10G) and NAA10 p.(L11R) Variants Hamper Formation of the NatA N-Terminal Acetyltransferase Complex. International journal of molecular sciences 3 33255974
2024 NAA10 gene related Ogden syndrome with obstructive hypertrophic cardiomyopathy: A rare case report. Medicine 2 38335407
2023 Clinical manifestations in a Chinese girl with heterozygous de novo NAA10 variant c. 247C > T, p. (Arg83Cys): a case report. Frontiers in pediatrics 2 37441566
2023 A four-year-old girl with pathogenic variant in the NAA10 gene and precocious puberty - case report and literature review. Annals of agricultural and environmental medicine : AAEM 2 38940118
2026 Generation of a male isogenic pair and a female isogenic pair(R83C) for studying NAA10-related syndrome as part of a large Ogden syndrome biobank. Stem cell research 1 41548501
2025 Cardiological Manifestations in Males and Females Affected by NAA10 -Related Disease. American journal of medical genetics. Part A 1 40304357
2025 NAA10 (N-Alpha-Acetyltransferase 10): A Multifunctional Regulator in Development, Disease, and Cancer. Cells 1 40558489
2022 A Case of NAA10-related Syndrome With Prolonged QTc Treated With a Subcutaneous Implantable Cardioverter Defibrillator After Ventricular Fibrillation. CJC pediatric and congenital heart disease 1 37969489
2026 UBE2M promotes malignant phenotypes of prostate cancer through mediating NAA10 neddylation. Journal of translational medicine 0 41857595
2026 Phenotypic variability in female individuals with the NAA10 missense variants p.(L126R), p.(L126V), or p.(F128L) leading to NAA10-related syndrome. Molecular and cellular pediatrics 0 41973310
2026 mTOR-NAA10-C7orf50 axis senses nutritional status to coordinate ribosome biogenesis and autophagy. Science advances 0 42139339
2026 NME3 Interacts With NAA10 to Promote RUNX2 Nuclear Translocation and Odontogenic Differentiation in Human Dental Pulp Stem Cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 42165278
2026 NAA10 and BTRC drive CREBRF degradation in endoplasmic reticulum stress and renal tubular injury. Journal of diabetes investigation 0 42262012
2025 Assessment of the preventive effect of knockdown of cellular genes NXF1, PRPS1PRPS1 and NAA10 in influenza infection in an in vitro model. Voprosy virusologii 0 40233338
2025 Functional evaluation of NAA10 variants in patients with Ogden syndrome. Psychiatric genetics 0 41384780
2024 Evaluating possible maternal effect lethality and genetic background effects in Naa10 knockout mice. bioRxiv : the preprint server for biology 0 37163119
2019 The N-end rule pathway enzyme Naa10 supports epiblast specification in mouse embryonic stem cells by modulating FGF/MAPK. In vitro cellular & developmental biology. Animal 0 30993557

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