Ask about this productRelated genes to: SORD antibody
- Gene:
- SORD NIH gene
- Name:
- sorbitol dehydrogenase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: SORD antibody
Related articles to: SORD antibody
- To develop an assay to measure red blood cell (RBC) sorbitol dehydrogenase (SORD) activity for fast laboratory screening of SORD-related neuropathies, and to provide additional phenotypic arguments in case of ambiguous genetic results. - Source: PubMed
Moro NicholasFrancois StanislasGrondin ChristelBen Salem SirineRajagopal SreekanthAykut DuruArezki LouisaLarramendi José ManuelBerquet ClaireWillems MarjolaineBouchet-Séraphin CélineGauthier Lucas WKonyukh MarinaSvahn JulietteMoutereau StéphanePeoc'h KatellTard CélineFernández-Eulate GorkaStojkovic TanyaBruneel ArnaudRaynor Alexandre - - Source: PubMed
Publication date: 2026/04/16
Taoka ToshiakiIto RintaroIwamoto KunihiroMiyata SeikoNakamichi ReiNakane ToshikiIima MamiFujishiro HiroshigeIkeda MasashiIchikawa KazushigeKamiunten AkifumiIchinose NobuyasuTanaka YoshikiNaganawa Shinji - Neuroblastoma (NB) progression is influenced by metabolic and redox adaptations. The polyol pathway, driven by aldose reductase (AKR1B1) and sorbitol dehydrogenase (SORD), is activated in hyperglycemic conditions, while detoxification of lipid peroxidation products such as 4-hydroxynonenal (4-HNE) involves carbonyl reductase 1 (CBR1) and AKR1B1. A systematic characterization of these enzymes under distinct metabolic and oxidative challenges in NB is currently lacking. - Source: PubMed
Publication date: 2026/02/27
Avanatti MartinaSardelli GemmaMosca RossellaBalestri FrancescoSignore GiovanniFelice FrancescaDel Corso AntonellaMoschini Roberta - Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer (NSCLC), and epidermal growth factor receptor (EGFR) mutation is its primary molecular driver event. Although the third-generation tyrosine kinase inhibitors (TKIs) Osimertinib has become the standard first-line therapy for such patients, the development of drug resistance severely limits long-term survival benefits. However, increasing evidence suggests that epigenetic remodeling is a crucial non-genetic mechanism contributing to resistance. Specifically, hypermethylation of DNA promoter regions can assist tumor cells in evading drug cytotoxicity by silencing key tumor suppressor genes or metabolic regulatory genes. This study aims to identify key genes regulating Osimertinib sensitivity through machine learning and high-throughput screening, and to dissect the role of methylation modifications in regulating primary resistance to Osimertinib. - Source: PubMed
Liang GuoweiWu HongfengJia ChaoyiGao PenghuZhang ZhanruiChen ChenLi YongwenLiu HongyuChen Jun - - Source: PubMed
Publication date: 2026/02/25
Kakal TasneemElkarib Asha Khalil AbdallaKusters LincieKok Maryse