Ask about this productRelated genes to: ALDH3A2 antibody
- Gene:
- ALDH3A2 NIH gene
- Name:
- aldehyde dehydrogenase 3 family member A2
- Previous symbol:
- SLS, ALDH10
- Synonyms:
- FALDH
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-14
- Date modifiied:
- 2018-05-03
Related products to: ALDH3A2 antibody
Related articles to: ALDH3A2 antibody
- The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is a master regulator of the cellular antioxidant response that defends against ferroptosis and facilitates tumour development. Here, by performing an aldehyde dehydrogenase (ALDH) family shRNA screen, our study identifies aldehyde dehydrogenase 3 family member A2 (ALDH3A2) as a potent NRF2 activator that inhibits ferroptosis. Interestingly, ALDH3A2 efficiently activates NRF2 in both wild-type (WT) Kelch-like ECH-associated protein 1 (KEAP1) and mutant KEAP1 tumour cells. Mechanistically, ALDH3A2 inhibits the phosphorylation of glycogen synthase kinase 3 beta (GSK3β) and blocks recruitment of E3 ubiquitin ligase beta-transducin repeat-containing protein (BTRC) to NRF2, thereby stabilizing NRF2 by preventing its proteasomal degradation. Knockdown of ALDH3A2 significantly promotes the activation of the GSK3β signaling pathway and accelerates NRF2 degradation. ALDH3A2 stabilizes NRF2 independently of its enzymatic activity, as enzymatic inactivation of ALDH3A2 fails to block ALDH3A2-mediated NRF2 activation and ferroptosis suppression both in vitro and in vivo. Taken together, our study reveals a novel NRF2 regulatory pathway and suggests ALDH3A2 as a promising druggable target for KEAP1-mutant tumours. - Source: PubMed
Publication date: 2026/08/17
Yang LiZhuang XiaoHan JingCui WeiweiZhang YudanWang ZiqiSong DandanZhou ChaoHuang ShaohuiCui KaiLin ChenchenXu MinZhao XingruWang ShuaiHuang BinWang HuiShi ShuangDu LutaoLuo QiankunZhang QunchengMa ZehengYin ChengqianChu BoZhang Xiaoju - Extremely rare cases show co-occurrence of Sjogren-Larsson syndrome (SLS) and central precocious puberty (CPP), and our understanding of it is still limited. In this case report, we reported a 9-year-old boy (weight: 20 kg; height: 120 cm) showing SLS and CPP simultaneously. The patient presented to our hospital with testicle enlargement and presence of pubic hair. SLS was diagnosed based on the presence of ichthyosis and intelligent disability, together with genetic confirmation by next-generation sequencing, which identified two pathogenic variants ( and ) in the gene. The diagnosis of CPP was established based on mildly advanced bone age, ultrasonographic evidence of pubertal development, and elevated basal gonadotropin and testosterone levels. The patient subsequently received triptorelin acetate (3.75mg) for treating CPP, while merely moisturization and rehabilitation was used for treating SLS. In the follow-up, he showed growth delay, with a body height of 120 cm at age 8.5 years old and 123.5 cm at 9.5 years old. - Source: PubMed
Publication date: 2026/07/21
Zhao CanmiaoTao NaGe LipingSun MeiyuanSu YanfangYang YangXu FangHuang QiXu Lijun - To characterize the clinical features and genetic spectrum of Chinese patients with Sjögren-Larsson syndrome (SLS). - Source: PubMed
Publication date: 2026/07/16
Chen FengYu BowenWang YangshuoYuan LiuZhang LiweiLiu TinghongZhai FengXu JinshanNi XinLiang Shuli - Endometritis is an inflammatory endometrium condition affecting reproductive outcomes. However, the pathology of endometritis is poorly understood. Thus, we attempted to investigate the pathogenic mechanism of endometritis and discover potential biomarkers. Transcriptome sequencing was performed on endometritis patient-derived endometrial tissues (n = 3) and normal controls (n = 5). Differentially expressed genes (DEGs) between disease and control groups were identified. Mitochondrial genes were filtered based on MitoCarta3.0. Small RNA sequencing (9 disease samples vs. 6 controls) was combined with differentially expressed (DE) mitochondrial genes to generate a competing endogenous RNA (ceRNA) network, followed by protein-protein interaction network analysis. Metabolome analysis was conducted to explore differentially expressed metabolites (4 cases vs. 4 controls). Comparative analysis revealed a total of 1,507 DEGs in disease group relative to controls, which were implicated in adaptive immune response, cell chemotaxis, and chemotaxis signaling pathways. In total, 28 mitochondrial genes were differentially expressed and mapped to the ceRNA network. ALDH3A2, ACSS3, CYP24A1, and KMO were identified as hub genes and were closely associated with the infiltration of CD8 T cells. CYP24A1 was found to be the target of four drugs, including calcitriol and deferasirox. Five metabolic pathways were significantly enriched, including the citrate cycle (TCA cycle) and taurine and hypotaurine metabolism. ALDH3A2, ACSS3, and KMO showed interactions with metabolites and significant pathways. Hub genes (ALDH3A2 and ACSS3) play critical roles in the pathogenesis of endometritis by interacting with different metabolites. Our study offers candidate biomarkers for diagnosing and treating endometritis. - Source: PubMed
Publication date: 2026/07/15
Xu AnranChen YanyanZheng YanjunWen YanSun YanyanDong FangdiYang HuijunFan YuanyuanYu Xuan - Oral lichen planus (OLP), a chronic inflammatory condition, is classified as a potentially malignant disorder due to its risk of progression to oral squamous cell carcinoma (OSCC). Mitochondrial metabolism plays a key role in pathogenesis and progression of OSCC. This study aimed to identify and validate biomarkers associated with mitochondrial metabolism-related genes (MRGs) in OLP and OSCC, thereby contributing to the development of novel therapeutic strategies. Transcriptomic data from OLP (GSE38616, GSE52130) and OSCC (GSE30784, GSE25099) datasets were analyzed. Differentially expressed genes were intersected with known MRGs to identify candidate biomarkers. These genes were further validated through expression analyses within the respective datasets. A predictive nomogram was constructed based on selected biomarkers and assessed for diagnostic performance. Functional enrichment analysis, immune cell infiltration profiling, pharmacological targeting prediction, molecular docking, and reverse transcription quantitative PCR (RT-qPCR) validation were performed to elucidate underlying biological mechanisms. Three biomarkers ALDH3A2, CYP11A1, and IMPDH2 were identified as significantly associated with both OLP and OSCC. Expression levels of these genes were significantly reduced in affected tissues compared to unaffected control tissues, a finding confirmed through RT-qPCR analysis. A nomogram incorporating these biomarkers effectively predicted OSCC risk. Functional enrichment analysis indicated co-enrichment of these genes in the olfactory transduction pathway in OLP and the ECM-receptor interaction pathway in OSCC. Analysis of immune infiltration identified 22 differentially abundant immune cell types in OSCC versus control samples, with ALDH3A2 exhibiting a strong inverse correlation with natural killer T cell levels. A total of 29 candidate compounds targeting these biomarkers were identified; among them, IMPDH2 presented a binding energy of - 10.6 kcal/mol with AC1NRCGS, indicating potential therapeutic relevance. ALDH3A2, CYP11A1, and IMPDH2 were validated as potential biomarkers linked to mitochondrial metabolism in patients with OLP and OSCC. These findings provide a foundation for further exploration of targeted treatment strategies in the management of OLP and OSCC. - Source: PubMed
Publication date: 2026/07/08
Wang QingmeiLin FeiWang XueyingGuan WeiqunChen Weihui