Ask about this productRelated genes to: ALDH3A1 Blocking Peptide
- Gene:
- ALDH3A1 NIH gene
- Name:
- aldehyde dehydrogenase 3 family member A1
- Previous symbol:
- ALDH3
- Synonyms:
- -
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-11-18
Related products to: ALDH3A1 Blocking Peptide
Related articles to: ALDH3A1 Blocking Peptide
- Air pollution exposure is increasingly recognized as a risk factor for chronic kidney disease (CKD), but the underlying mechanisms, especially the complex gene-environment interactions as reflected in genetic susceptibility, transcriptomic, and proteomic signatures, remain to be elucidated. - Source: PubMed
Publication date: 2026/05/09
Lu JianSun ShuaigangShang XinruDeng ZekaiWang ShunweiJiang ShiminLi Wenge - Cigarette smoking remains one of the leading causes of preventable death worldwide. Upon inhalation, smoke induces damage to the lung epithelium, which can be the driving force for the development of chronic lung diseases. In the current study, we identified the "smoking signature" by assessing transcriptomic differences between current and non-smokers in multiple cohorts. By mapping the smoking signature onto single-cell and spatial transcriptomics data, we identified the surface layer of the airway epithelium as the part of the airways most affected by smoke. Next, by comparing the smoking signature between lungs of humans and non-human primates, we identified a cluster of human-specific smoke-response genes, suggesting an evolutionary adaptation to smoke exposure. Methylation and ChIP-seq analyses were used to identify and as master regulators of the smoking signature. Knockout of smoking signature-genes and revealed their role in protective responses of the airways upon smoke exposure. - Source: PubMed
Publication date: 2026/04/01
Pouwels Simon DChen HaoRathnayake Senani N HLan AndyMahbub Rashad MYeung Anna Chi YingBrandsma Corry-AnkeLobo Thamar JGuryev VictorHeijink Irene Hvan den Berge MaartenFaiz Alen - Sepsis triggers a complex and heterogeneous host response, yet decades of biomarker studies have yielded few targeted therapeutics that improve patient outcomes. Single analyte approaches fail to capture the coordinated biological programs that drive organ dysfunction. Focusing on single or limited panels of biomarkers to endotype disease fundamentally misrepresents sepsis biology, which reflects simultaneous disruption of multiple cellular networks. However, pathway-level bioinformatic analyses interpret proteins as components of larger biological systems, enabling detection of coordinated molecular disturbances that individual biomarkers cannot capture. - Source: PubMed
Publication date: 2026/04/02
Van Nynatten Logan RTweddell DavidDaley MarkCepinskas GediminasBasmaji JohnSlessarev MaratFraser Douglas D - Salivary aldehyde dehydrogenases (ALDHs), particularly ALDH3A1 and ALDH1A1, serve as frontline enzymatic defenses in the oral cavity, detoxifying reactive aldehydes generated through metabolic activity, microbial fermentation, and environmental exposures. These enzymes are essential for maintaining redox homeostasis, mucosal integrity, and immune modulation. However, under chronic metabolic stress, such as in diabetes, oral inflammation, and cancer, salivary ALDHs become vulnerable to non-enzymatic glycation by reactive carbonyl species like methylglyoxal. This modification impairs cofactor binding, catalytic activity, and structural stability, thereby compromising detoxification capacity at a time of heightened aldehyde burden. This review provides the first insights into ALDH glycation and particularly that of salivary ALDH, examining its structural mechanisms, disease-specific consequences, and emerging protective strategies. Special focus is given to natural compounds, including curcumin, thymoquinone, resveratrol, carnosine, and EGCG, that prevent glycation or restore ALDH function via carbonyl scavenging, antioxidant activation, and NAD/SIRT1 pathway modulation. We also highlight critical research gaps, such as the absence of site-specific glycation maps, lack of salivary gland-based models, and limited availability of ALDH3A1-specific activators. Importantly, we propose that the glycation status of salivary ALDHs may serve as a non-invasive biomarker of oxidative stress and therapeutic response in metabolic and inflammatory disorders. By bridging biochemical insights with translational potential, this review establishes ALDH glycation as a mechanistic and clinically actionable axis in oral and systemic health. - Source: PubMed
Publication date: 2026/03/12
Khan Masood AlamYounus Hina - Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder shaped by genetic and environmental factors. Phthalates, widely used as plasticizers in consumer products, have gained attention as potential environmental contributors to ASD; however, their pathogenic roles remain insufficiently defined. This study systematically investigated the molecular associations between three common phthalates, diethyl phthalate (DEP), dimethyl phthalate (DMP), and dioctyl phthalate (DOP), and ASD risk using integrated network toxicology and bioinformatics approaches. Intersection analysis of phthalate-associated targets and ASD-related genes revealed shared enrichment in lipid metabolism-related pathways. Protein-protein interaction network analysis identified 10 key targets: FAAH, CYP2C9, CYP24A1, ACHE, CYP11B1, TSPO, PTGS2, MIF, ADORA1, and ALDH3A1. Molecular docking and dynamics simulations indicated stable binding interactions between phthalates and the target. Mendelian randomization analysis further suggested that FAAH and ADORA1 serve as key pathogenic mediators linking phthalate exposure to ASD risk. In vivo experiments demonstrated that C57BL/6 mice exposed to individual or mixed phthalates exhibited ASD-like behaviors, including reduced social interaction, increased repetitive behaviors, and cognitive impairment, with the most pronounced effects observed in the DEP, DMP, and mixed exposure groups. qRT-PCR analysis of hippocampal tissue showed significant downregulation of Faah and upregulation of Adora1 in the DEP group. Collectively, these findings identify FAAH and ADORA1 as central molecular links between phthalate exposure and ASD-related phenotypes from a systems toxicology perspective, providing insight into environmental contributions to neurodevelopment and potential molecular targets for intervention. - Source: PubMed
Publication date: 2026/03/25
Sun YaoLyu LiangZhang XiruiChen ShuangshuangLiu YutongQiao WanyingZhu TikangWang ShutingWang ZuyueZhou DingHai YangFan Lili