Ask about this productRelated genes to: ALDH3A2 Blocking Peptide
- 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 Blocking Peptide
Related articles to: ALDH3A2 Blocking Peptide
- Abdominal fat thickness (AFT) is a crucial indicator for assessing fat deposition in White Feather broilers. Previous genome-wide association studies (GWAS) have primarily focused on single-point measurements of abdominal fat, with limited attention given to longitudinal phenotype records. Compared to traditional GWAS models, the longitudinal data-based GWAS (LONG-GWAS) model accounts for temporal phase effects, thereby more effectively controlling the false positive rate. This study conducted a genome-wide association analysis on 1654 White Feather broilers at four distinct ages during the laying period of broiler breeders (25, 27, 35, and 43 weeks). Three SNP loci associated with fat were identified (rs16341267, rs740644432, and rs15049519), which were annotated to three candidate genes: FDFT1, HTR2C, and ALDH3A2. These genes are involved in regulating lipid metabolism, energy balance, and fat deposition. This study provides new insights into the genetic basis of abdominal fat thickness in White Feather broilers and offers stage-specific marker information that can accelerate precision breeding for abdominal fat control in white feathered broilers. - Source: PubMed
Li PenghaoLuo NaYing FanZhu DanLiu DaweiSong XianyiWen JieZhao GuipingAn Bingxing - Inborn errors of metabolism (IEM) are frequently underdiagnosed in low-resource settings due to limited diagnostic infrastructure. We hypothesized that an integrated clinical-genomic approach could improve diagnosis and management of these conditions. Nineteen Pakistani families with clinically suspected IEM underwent systematic clinical assessment, available biochemical testing, and whole-exome sequencing (WES). Variants were classified according to ACMG/AMP guidelines using evidence from population databases, in silico prediction tools, segregation analysis, and genotype-phenotype correlation. Clinical diagnoses and management strategies were reassessed based on molecular findings. WES provided a molecular diagnosis in 90% (17/19) of families and enabled targeted therapeutic interventions in 70% (13/19). However, clinical outcomes were variable due to advanced disease in some cases and limited follow-up. Seven novel variants were identified in CYP27B1, DYM, MTTP, ALDH3A2, USP53, BRAF, and JAG1, while twelve recurrent mutations were detected in PIGN, GCDH, CLCN7, RNASEH2C, ABCB11, MPV17, IDUA, SMPD1, FBP1, SLC37A4, ACADM, and UGT1A1. Integrating genomic findings with clinical reassessment improved diagnostic precision. An integrated clinical-genomic approach enabled accurate diagnosis of pediatric IEM in resource-limited settings, with particular utility in children with metabolic disorders in a consanguineous population. Identification of both novel and recurrent variants expanded the genotypic and phenotypic spectrum of these disorders and highlighted the clinical utility of genomic diagnostics in optimizing patient care. - Source: PubMed
Publication date: 2026/04/13
Mansoor SumreenaAbid SabeenImran MuhammadMalik Munir IqbalAli QamarHussain ShanawazAli Hafiz AsimMasood YasserChoudhry ShehlaQamar RaheelAzam Maleeha - Diabetes elevates the risk of ischemic stroke and poor prognosis. Exosomes, which carry nucleic acids and proteins, transmit stable signals across the blood-brain barrier and serve as promising non-invasive biomarkers for brain injury. Exosome proteomics may thus reveal novel therapeutic strategies to improve outcomes in diabetic stroke patients. Exosomes were isolated from the plasma of acute ischemic stroke patients with and without type 2 diabetes (n = 10 each) and characterized them using electron microscopy, flow cytometry, and nanoparticle tracking analysis. Label-free proteomics and bioinformatics were performed to identify prognostic biomarkers, with mass spectrometry data deposited in ProteomeXchange (PXD068810). CIBERSORTx and BRETIGEA were used to resolve cellular origins, and western blotting was applied to verify key proteins in mouse brain tissue and plasma exosomes after stroke. Diabetic stroke patients showed higher glucose, HbA1c and neutrophils. Proteomics identified 95 differentially expressed proteins mainly involved in oxygen/NO transport, glucose metabolism and oxidative stress. Protein-protein interaction network analysis highlighted HBA1, HBA2, HBB, HBD, PFKL, and ALDH3A2 as key regulators. Western blot confirmed that db/db mice brain exhibited significantly elevated HBA2 and HBB, reduced PFKL expression which correlated with MAP2 at 24 h after reperfusion. Plasma-derived exosomes from db/db mice also showed markedly lower PFKL expression. Diabetes altered exosomal contributions, diminishing signals from CD4 memory T cells and brain endothelial cells, while enhancing those from follicular helper T cells. These findings underscore the potential of exosome-based diagnostics and therapeutics for diabetic stroke, paving the way for innovative therapeutic strategies. - Source: PubMed
Publication date: 2026/04/08
Jiang QianPeng GuanggeKong QiZhou YingnanZhao HaipingGeng Xiaokun - was previously found to be the dominant genus of a hydrocarbon-degrading, diesel-enriched microbial consortium from oil-spill contaminated soils in Guimaras Island, Philippines. However, the species-level identity, individual degradation efficiency, and genomic determinants of metabolic pathways and environmental stress adaptation remain unknown, limiting the understanding of the ecological role and bioremediation potential of species. This study isolated, characterized, and evaluated the hydrocarbon degradation efficiencies of species from the consortium. From 110 putative colonies, 11 isolates showed significantly different degradation capacities of at least 66% on diesel, hexane, hexadecane, and xylene, suggesting diversity at the species and strain level, and substrate preference. Isolate KLMG-HD-125 demonstrated complete oxidative degradation of short- and mid-chain n-alkanes (C11-C25) in diesel, indicating a broad substrate range and strong petroleum degradation potential. Whole genome sequence analysis confirmed the identity of KLMG-HD-125 as with a genome size of 5.55 Mb and GC content of 57.2%. It harbors genes responsible for alkane and xylene degradation, and pathways to respond to oxidative, membrane, and solvent stress, indicating ecological fitness, allowing the isolate to remain metabolically active in potentially toxic petroleum-impacted environments. Specifically, the presence of (LadA-like FMN-dependent monooxygenase), (primary alcohol dehydrogenase), and (long-chain aldehyde dehydrogenase) indicates the pathway for terminal oxidation of alkanes. Although 11 virulence-associated genes were identified in KLMG-HD-125, the hypervirulence determinants were absent. Together with its environmental origin, these findings indicate that KLMG-HD-125 is potentially opportunistic rather than an obligate pathogen. Overall, KLMG-HD-125 is equipped with phenotypic and genomic traits essential for hydrocarbon remediation, specifically of n-alkanes, and ecological fitness to persist in petroleum-impacted environments, though its potential pathogenicity requires careful biosafety assessment prior to environmental application. - Source: PubMed
Publication date: 2026/03/18
Garcia Kalel Liam MAlemania Darlene Kris VOpulencia Rina B - - Source: PubMed
Publication date: 2026/04/01
Ali Muhammad ZeeshanSattar SamiaAlayoubi Abdulfatah MAbbas ShakilAlharthi Mohammed Turki HussainAltemani Alwaleed Fahad HLatif MuhammadKhan Muzammil AhmadWindpassinger Christian