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
- Triphenyltin chloride (TPTC), a member of the organotin family, has been widely restricted due to its endocrine-disrupting effects. Nevertheless, TPTC continues to be detected in aquatic environments and poses potential health risks owing to its persistence and bioaccumulation. Although previous studies have shown that triphenyltin compounds can disrupt lipid homeostasis through nuclear receptor pathways involving retinoid X receptor (RXR) and peroxisome proliferator-activated receptors (PPARs), whether TPTC exerts hepatocytotoxicity through direct metabolic targets remains unclear. This study employed a metabolomics-driven target discovery strategy to analyze intracellular metabolite extracts from HepG2 cells exposed to TPTC for 24 h, aiming to investigate the underlying molecular mechanisms of TPTC-induced metabolic toxicity. Untargeted global metabolomics analysis revealed that TPTC exposure caused significant disturbances in hepatic lipid metabolism, characterized by the accumulation of medium- and long-chain fatty acids and depletion of key metabolites associated with fatty acid β-oxidation. Pathway enrichment analysis and protein-protein interaction network analysis further indicated that two mitochondrial dehydrogenases involved in fatty acid catabolismhydroxysteroid 17β-dehydrogenase 10 (HSD17B10) and hydroxyacyl-CoA dehydrogenase (HADH)are potential metabolic targets responsible for the observed alterations. Molecular docking, surface plasmon resonance, and cellular thermal shift assays confirmed direct interactions between TPTC and both HSD17B10 and HADH, with binding affinities at the micromolar level. Functional validation demonstrated that TPTC disrupts mitochondrial respiratory function and redox balance by interfering with HADH- and HSD17B10-dependent generation of acetyl-CoA and NADH, leading to mitochondrial dysfunction and oxidative stress. In summary, this study reveals a previously underappreciated mechanism of TPTC toxicity involving mitochondrial metabolism, extending the current understanding of its toxicological pathways beyond nuclear receptor-mediated signaling to include direct disruption of mitochondrial energy and redox metabolism. - Source: PubMed
Publication date: 2026/05/07
Wang YanweiZhao JiahuiPan ShanshanLiu XuesongChen YongXu TengfeiFang Mingliang - Lung cancer (LC) and venous thromboembolism (VTE) are closely associated, with VTE contributing to morbidity and mortality among patients with LC. We aimed to identify and characterize a mitochondrial-related transcriptomic signature shared between LC and VTE and to explore its association with immune microenvironment features. - Source: PubMed
Publication date: 2026/09/04
Zhang Xue LiGao Ai LiLiu Zhan Ju - Leishmaniasis is one of the most prominent worldwide flagellated protozoan parasite diseases. Natural products have gained attention as potential anti-leishmanial agents due to their fewer side effects, low toxicity, and cost effectiveness compared to conventional chemotherapy drugs. In the current study, the network pharmacology approach was used to evaluate the therapeutic potential of derived phytochemicals against Leishmaniasis and toidentify potential anti-leishmanial agents targeting key proteins implicated in leishmaniasis progression.To carry out this study, several databases including Cytoscape, IMPPAT, Dr. Duke's, Kyoto Encyclopaedia of Genes and Genomes (KEGG), and STRING database, were used to conduct network pharmacology to examine the biomolecular approach of metabolites of the plant in leishmaniasis disease. A total of 33 phytochemical components from were analyzed, resulting in the identification of five major bioactive molecules: betulinic acid, betulin, lupeol, oleanolic acid, and karachic acid. These compounds had high affinity for a variety of leishmaniasis-related molecular targets, including MAPK1, NFKB1, TLR4, HSD17B10, and DHODH, among others. A protein-protein interaction (PPI) network was created to identify essential connections, and Gene Ontology (GO) and KEGG pathway enrichment studies revealed their involvement in inflammation, immunological regulation, and apoptotic pathways. Among these metabolites, betulin and betulinic acid were found to be the most active metabolites with the most prominent interaction with the genes that play an active role in the pathophysiology of leishmaniasis. may be identified potential source of anti-leishmanial drug candidates. - Source: PubMed
Publication date: 2026/01/06
Loshali AanchalSaifi SumailaJoshi Bhuwan ChandraBawa SandhyaAeri Vidhu - 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