Human Glyoxalase II / HAGH Protein
- Known as:
- Human Glyoxalase II / HAGH Protein
- Catalog number:
- HAH-H5121
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human Glyoxalase / HAGH Protein
Ask about this productRelated genes to: Human Glyoxalase II / HAGH Protein
- Gene:
- HAGH NIH gene
- Name:
- hydroxyacylglutathione hydrolase
- Previous symbol:
- -
- Synonyms:
- GLO2, GLXII, HAGH1
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-08-25
Related products to: Human Glyoxalase II / HAGH Protein
Related articles to: Human Glyoxalase II / HAGH Protein
- Radiation pneumonitis (RP) is a dose-limiting toxicity in lung cancer radiotherapy, often poorly predicted by static clinical and dosimetric models. We aimed to identify a robust, blood-based proteomic signature grounded in the longitudinal biological response to radiation to enable accurate, early risk stratification. - Source: PubMed
Publication date: 2026/05/22
Lingyun WuNakamura MasakiToru MukoharaJing YangZeyu SunChunyun RenDeying ChenKan JiangQiuying TangKaikai DingXin YinHao YuYuzheng ZhouSiyuan WangJie YinYongheng YanYu HeQuanhai LiWeiWei Zhongjie LuXiaoli SunChiyuan MaXianghua YeSenxiang Yan - Epilepsy is a common neurological disorder with high genetic heterogeneity and affects approximately 70 million people worldwide. Although several studies have combined Genome-Wide Association Studies (GWAS) with bulk expression quantitative trait loci (eQTLs) to explore epilepsy risk genes, the cellular context of genetic regulation remains insufficiently defined. - Source: PubMed
Publication date: 2026/04/21
Zhong Gao-YangLiu CongWang Hui-LingLiang ManLiu Zi-Long - Long COVID is a complex condition where symptoms persist for more than 3 months after SARS-CoV-2 infection and affects an estimated 5-30% of individuals. While persistent inflammation has emerged as an important feature of this condition, it is unclear if immune responses from COVID-19 vaccination or SARS-CoV-2 re-infection exacerbate or mirror the initial inflammatory responses. - Source: PubMed
Publication date: 2026/04/13
Bansal AmitOlechnowicz Sam W ZKiernan-Walker NicholasCumming JacobAbdul Azeez ImadhMazhari Ramin Cox Rebecca JMueller IvoBowden RoryEriksson Emily M - Mitochondrial dysfunction contributes critically to epileptogenesis. Therefore, identifying key mitochondrial function-associated genes in epilepsy may provide novel insights into its pathogenesis. We employed expression quantitative trait loci (eQTLs) and Mendelian randomization analyses to assess mitochondrial-epilepsy causality, with leave-one-out validation confirming the reliability and directionality of the results. The results revealed that hydroxyacylglutathione hydrolase (HAGH), oxysterol-binding protein-related protein 1A (OSBPL1A) and pantothenate kinase 2 (PANK2) were pivotal epileptogenic genes. HAGH modulates the mechanistic target of rapamycin complex 1 (mTORC1) signaling and fatty acid metabolism pathways. OSBPL1A mediates apoptotic and reactive oxygen species (ROS) pathways. PANK2 regulates phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling and Notch signaling cascades. Additionally, these genes participate in inflammatory pathways, including T cell receptor (TCR), mitogen-activated protein kinase (MAPK), and tumor necrosis factor (TNF) signaling. We demonstrated that HAGH, OSBPL1A, and PANK2 constitute core pathogenic mechanisms in epilepsy. These genes potentially govern epileptogenesis through mitochondrial regulation via neuroinflammatory, immunomodulatory, and apoptotic pathways. Our findings provide a foundation for investigating epileptogenesis, discovering therapeutic targets, and identifying prognostic biomarkers. - Source: PubMed
Publication date: 2026/03/09
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