ARD1A
- Known as:
- ARD1A
- Catalog number:
- 001833A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARD1A
Related genes to: ARD1A
- Gene:
- NAA10 NIH gene
- Name:
- N(alpha)-acetyltransferase 10, NatA catalytic subunit
- Previous symbol:
- ARD1, ARD1A
- Synonyms:
- DXS707, TE2
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-29
- Date modifiied:
- 2017-12-15
Related products to: ARD1A
anti-ARD1Aanti-ARD1Aanti-ARD1Aanti-ARD1Aanti-ARD1A (4B7-H4)anti-ARD1A type: Primary antibodies host: Mouseanti-ARD1A type: Primary antibodies host: RabbitARD1,ARD1A,Homo sapiens,Human,NAA10,N-alpha-acetyltransferase 10,NatA catalytic subunit,N-terminal acetyltransferase complex ARD1 subunit homolog A,TE2Ard1,Ard1a,Mouse,Mus musculus,Naa10,N-alpha-acetyltransferase 10,NatA catalytic subunit,N-terminal acetyltransferase complex ARD1 subunit homolog A,Te2ARD1A (C_term)ARD1A (C_term)ARD1A (Human) Matched Antibody PairARD1A (Human) Matched Antibody Pair ab pairsARD1A 293T Cell Transient Overexpression Lysate(Denatured)ARD1A 293T Cell Transient Overexpression Lysate(Denatured) Related articles to: ARD1A
- Triple-negative breast cancer (TNBC) poses a significant clinical challenge due to its aggressive nature and lack of targeted therapies. A subset expressing the Androgen Receptor (AR) offers a therapeutic opportunity, yet the mechanisms remain incompletely understood. Breast cells were cultured under hormone-deprived or androgen-stimulated conditions with or without AR inhibitors. Short hairpin RNA knockdown or overexpression of AR, ARD1, and DLGAP5 was performed. Functional assays included CCK-8, colony formation, migration and invasion, and apoptosis by flow cytometry. Protein interactions and transcriptional regulation were examined using co-immunoprecipitation and chromatin immunoprecipitation. In vivo, xenograft models of TNBC were established in BALB/c nude mice. Clinical relevance was validated using paired TNBC and adjacent normal tissues. AR and ARD1 were co-upregulated in AR+ TNBC cells and tissues, correlating with poor prognosis. ARD1 promoted TNBC malignant phenotypes in vitro and in vivo. Mechanistically, androgens induced ARD1 protein stabilization via AR. ARD1 physically interacted with AR, enhanced AR acetylation, and potentiated AR transcriptional activity. DLGAP5 was identified as a transcriptional target co-regulated by AR and ARD1. DLGAP5 upregulation promoted tumor growth and drove expression of the immune checkpoint ligand PD-L1 via signal transducer and activator of transcription 3, suppressing cytotoxic T-cell marker expression. In vivo, DLGAP5 overexpression accelerated tumor growth and increased PD-L1; treatment with an AR PROTAC reversed these effects. ARD1 acts as a critical AR coactivator, driving DLGAP5 expression, which subsequently promotes tumor progression and immune evasion through PD-L1 upregulation. Targeting the AR/ARD1/DLGAP5 axis represents a promising therapeutic strategy for this breast cancer subtype. - Source: PubMed
Publication date: 2026/09/16
He ChongwuZhou BinChen JingTian RuiboZeng XiaoqiangWan XianghuaYu TenghuaZou Jun - N-terminal acetylation (NTA) is a ubiquitous eukaryotic post-translational modification catalyzed by Nα-acetyltransferases (NATs). Among the eight NAT families, the NatA complex-composed of the catalytic subunit NAA10 and auxiliary subunit NAA15-mediates N-terminal acetylation of ~40% of mammalian proteins. Pathogenic mutations in NAA10 or NAA15 disrupt NatA complex integrity or enzymatic activity, resulting in NAA10- or NAA15-related syndromes. Both disorders share overlapping clinical features, including developmental delay, intellectual disability, growth impairment, skeletal anomalies, and cardiac dysfunction. However, emerging clinical evidence highlights cardiac defects, particularly life-threatening arrhythmias and structural abnormalities, as the predominant phenotype contributing to the major cause of mortality in these syndromes. This review systematically dissects how distinct classes of NAA10 and NAA15 mutations perturb cardiac function through: (i) NatA complex assembly defects, (ii) catalytic dysfunction spanning impaired acetyltransferase activity and disrupted ribosome binding (iii) protein destabilization, and (iv) ion channel dysregulation, integrating clinical phenotypes with mechanistic insights from patient-derived iPSC-cardiomyocyte models and biochemical studies. We critically evaluate current methodologies and identify research gaps. Finally, we consider how mechanistic insights from these severe early-onset disorders-particularly regarding proteostasis failure and ion channel dysfunction-may extend beyond rare disease contexts to inform broader cardiac biology, including emerging concepts of proteostasis decline in cardiac ageing. - Source: PubMed
Publication date: 2026/09/16
Liu YutingSun LeiZhang HuanMa YijiaLi MiaoLi JianFeng Rui - Cell-free fetal mRNA (cff-mRNA) in amniotic fluid has emerged as a valuable source of molecular information reflecting fetal development. We aimed to identify cff-mRNA transcripts showing gestational-age-dependent expression patterns in human amniotic fluid and to characterize their expression changes across gestation. Cell-free mRNAs from amniotic fluid samples at 16 and 38 weeks' gestation (n = 1 each) were analyzed by RNA sequencing. Candidate mRNAs showing gestational-age-dependent transcriptional changes were selected based on an expression level of ≥300 transcripts per million (TPM) at either 16 or 38 weeks' gestation and a 38-week/16-week expression ratio of ≥20. As confirmation analysis, RT-qPCR was performed using independent amniotic fluid samples collected at 16 weeks' gestation (n = 20) and 38 weeks' gestation (n = 20). Overall, 1587 mRNAs were identified by RNA sequencing analysis. Among mRNAs showing gestational-age-dependent increases in expression, six candidate genes (SFTPC, NAA10, CALML5, SMIM29, IFITM3P6, and ARF-1) were selected for RT-qPCR validation based on expression changes and tissue representation. RT-qPCR confirmed that all six genes were significantly more highly expressed at 38 weeks than at 16 weeks (all p < 0.0001; Mann-Whitney U test). This study identified candidate cff-mRNAs in human amniotic fluid that exhibit gestational-age-dependent expression patterns. These findings provide preliminary insights into developmental transcriptional changes during fetal development and contribute to our understanding of the amniotic fluid transcriptome. Further validation of the findings obtained here in larger, independent cohorts is required. - Source: PubMed
Publication date: 2026/08/12
Eishi ChiakiMiura ShokoNagata KohNagata AiKitajima YurikoHasegawa YuriYoshiura Koh-IchiroMiura Kiyonori - Diabetic kidney disease (DKD) is a frequent complication associated with diabetes. CREBRF was reported to be closely associated with endoplasmic reticulum stress. However, the upstream regulatory mechanism by which CREBRF modulates endoplasmic reticulum stress in DKD renal tubular injury is unknown. - Source: PubMed
Publication date: 2026/06/09
Fang SitianNing JingHuang JinjingChen Yanxia - Human dental pulp stem cells (hDPSCs) hold great promise for dental tissue regeneration, yet the molecular mechanisms underlying their odontogenic differentiation remain unclear. This study investigates the role of nucleoside diphosphate kinase 3 (NME3) in regulating hDPSC differentiation. NME3 was found to be specifically expressed in odontoblasts of rat tooth germs and positively associated with odontogenic markers (DSPP, DMP1, and RUNX2) in hDPSCs. Functional assays revealed that NME3 promotes odontogenic differentiation, while its knockdown suppresses mineralization and marker expression. Mass spectrometry identified N-α-acetyltransferase 10 (NAA10) as a potential NME3-interacting protein, with both showing colocalization in hDPSCs and developing odontoblasts. Mechanistically, NAA10 knockdown rescued the differentiation deficits caused by NME3 silencing, and NAA10 overexpression attenuated the effects of NME3. Moreover, NME3 appears to facilitate the nuclear translocation of RUNX2, a key transcription factor in odontogenesis. These findings suggest that NME3 may regulate hDPSC odontogenic differentiation through interaction with NAA10 and modulation of RUNX2 localization, offering new insights into the molecular control of dental tissue regeneration. - Source: PubMed
Fan ChangxiuXu KeFei WenchaoLi YuejunZhao ShouliangJu Yanqin