ABAD _ HADH2 Antibody
- Known as:
- ABAD _ HADH2 Antibody
- Catalog number:
- AF1005a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ABAD _ HADH2 Antibody
Related genes to: ABAD _ HADH2 Antibody
- Gene:
- HSD17B10 NIH gene
- Name:
- hydroxysteroid 17-beta dehydrogenase 10
- Previous symbol:
- HADH2, MRXS10
- Synonyms:
- ERAB, MHBD, 17b-HSD10, ABAD, SDR5C1, MRPP2, CAMR
- Chromosome:
- Xp11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2019-04-23
Related products to: ABAD _ HADH2 Antibody
Related articles to: ABAD _ HADH2 Antibody
- Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by epidermal dysfunction, aberrant keratinocyte activation, and complex immune remodeling. Although lipid dysregulation has increasingly been implicated in psoriasis, the role of palmitoylation-associated genes in cutaneous inflammation remains insufficiently defined. - Source: PubMed
Publication date: 2026/07/21
Luo QingqiongShi RongcanYang DandanTang YijieXie QinghuiShi YulingSun Fenyong - The advent of the first disease-modifying therapies for Alzheimer's disease (AD) has renewed optimism for effective prevention and treatment strategies. Growing mechanistic insights indicate that AD pathogenesis is multifactorial and non-linear, better conceptualized as a circular vortex in which interconnected pathological processes reinforce one another. This complexity highlights the necessity for multiple druggable targets and combination-based therapeutic approaches. A hallmark of AD is reduced cerebral glucose utilization, revealed by positron emission tomography studies, reflecting profound metabolic disruption and mitochondrial dysfunction. Among mitochondrial candidates, 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10), encoded by HSD17B10, has emerged as a protein of interest. Despite debate surrounding its substrate specificity due to conflicting data, its elevated expression in neurons and astrocytes within AD brains underscores its potential relevance. This review outlines chemical entities targeting both catalytic and non-catalytic functions of 17β-HSD10 and examines whether its inhibition offers biological efficacy and clarifies its metabolic roles in the living brain. - Source: PubMed
Publication date: 2026/05/28
Kwa ErnstOgilvie Charlene EKormos Natalie CGreen Alison J ESmith Terry KGunn-Moore Frank J - High glucose is known to impair cognitive function in individuals with type 2 diabetes, though the precise mechanisms remain unclear. In this study, guided by lactylome analysis, we demonstrate that high glucose induces HSD17B10 K105 lactylation in hippocampal neurons by upregulating lactyltransferase Aars1, which reduces HSD17B10 enzyme activity, subsequently resulting in impaired breakdown and excessive accumulation of lipid droplets, and ultimately leading to neuronal apoptosis and cognitive decline. Notably, a short peptide that competitively inhibits HSD17B10 K105 lactylation remarkably mitigates cognitive impairment in diabetic mice. Furthermore, results from a large-scale prospective cohort study reveal that elevated plasma HSD17B10 K105 lactylation serves as an independent predictor of cognitive dysfunction in patients with type 2 diabetes. These findings uncover a critical pathway linking high glucose-induced lactylation to lipid accumulation and neuronal cell death, highlighting promising molecular targets for the prevention and treatment of diabetes-associated cognitive impairment. - Source: PubMed
Publication date: 2026/06/11
Xu JingxiCao JingxueYang XingHao YuqiGao YunSun XiaodongNie RongrongZhong QiongsuiZhong YuanmeiLeng ShaXu LuNie ChunxiaZheng Tianpeng - A series of novel naphtho[2,3-b]furan-4,9-dione derivatives were designed and synthesized as dual inhibitors targeting 17β-HSD10 and CDK5/p25. Through in vitro enzymatic inhibition assays, blood-brain barrier permeability prediction, and molecular docking analysis, derivative 5l was identified as a lead candidate and selected for further in vivo evaluation. Pharmacodynamic assessment in APP/PS1 transgenic mice demonstrated that 5l significantly improved cognitive performance in the Morris water maze test. Mechanistic studies revealed that 5l not only effectively ameliorated mitochondrial function, but also attenuated aberrant Tau phosphorylation, reduced Aβ deposition, inhibited neuroinflammation, and enhanced neurotrophic support. Western blot results indicated that the neuroprotective effects of 5l were not mediated by modulating the expression levels of 17β-HSD10 and CDK5, but rather through inhibiting their enzymatic activities. Collectively, these findings demonstrate that this class of dual inhibitors counteracts key pathological features of Alzheimer's disease through multi-target and multi-pathway synergy, providing a solid experimental foundation for the development of novel therapeutic agents for AD. - Source: PubMed
Publication date: 2026/04/17
Dao ShiyunCui ChaoHe WanqingLiu ErfengZhang LijunTang Huang - HSD10 mitochondrial disease (HSD10MD) is a rare X-linked disorder caused by pathogenic variants in the gene, encoding the mitochondrial enzyme 17β-hydroxysteroid dehydrogenase type 10 (HSD10). This enzyme is crucial for isoleucine degradation, neuroactive steroid metabolism, and mitochondrial function. HSD10MD typically presents in infancy or early childhood with severe neurodevelopmental regression, seizures, and cardiomyopathy, often leading to early mortality. Adult cases are extremely rare, with milder phenotypes associated with somatic mosaicism. - Source: PubMed
Publication date: 2026/02/26
Khodawrdi AlyaaMekki ChadiaLunati-Rozie ArianeFunalot Benoît