HADHSC Antibody
- Known as:
- HADHSC Antibody
- Catalog number:
- XW-8005
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HADHSC Antibody
Related genes to: HADHSC Antibody
- Gene:
- HADH NIH gene
- Name:
- hydroxyacyl-CoA dehydrogenase
- Previous symbol:
- HADHSC
- Synonyms:
- HADH1, SCHAD
- Chromosome:
- 4q25
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: HADHSC Antibody
Related articles to: HADHSC Antibody
- Cervical squamous cell carcinoma (CSCC) exhibits profound spatial heterogeneity in evolutionary trajectories across distinct tumour foci, yet the underlying mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/04/27
Lin ShitongLuo ZhihuiLi YutingHu BaiQu MinghanLiu BinghanCao CanhuiPeng TingXu MiaochunXu YashiLiu XiaojieWang XiaoliLi LiDing WenchengXu ZhenyuLi RuizhiZhao JingweiZhang JingminWang LingfangRen FangWang ChaolongWu Peng - Lysine lactylation (Kla) has emerged as a novel posttranslational modification implicated in various disease processes, yet its role in diabetic cardiomyopathy (DCM) pathogenesis remains unknown. The objective of this study was to ascertain whether protein lactylation is involved in DCM progression. - Source: PubMed
Ma DiCai WenjieYuan HuiShi MeixinJin YeCui YifengLiu PengLiu XiWei Can - Congenital hyperinsulinism (CHI) is the commonest cause of persistent hypoglycaemia in neonates and infants (blood glucose <3.0 mmol/L in first 2-3 days of life; <3.5 mmol/L after 3 days of life). Diazoxide demonstrates variable efficacy depending on the underlying genetic variant and clinical phenotype. Diazoxide has been associated with side effects that are likely dose dependent. This narrative review synthesizes current evidence on diazoxide's pharmacokinetics and side effect profile to support the development of individualised dosing strategies guided by genotype and patient-specific risk factors, with the aim of optimizing therapeutic outcomes and minimizing adverse effects. - Source: PubMed
Publication date: 2026/03/30
Wong TeresaChan DanielChua CherieCher WenqiLim SelinaChandran SureshYap Fabian - Lung transplantation serves as a life-saving therapeutic intervention for patients with end-stage pulmonary diseases, with the lung ischemia-reperfusion injury (LIRI) as the major challenge. Correcting lipid metabolic dysregulation in alveolar epithelial cells by targeting key causative molecules is a promising therapeutic strategy for LIRI. Quantitative proteomics and metabolomics revealed that dysregulated fatty acid metabolism dominates the LIRI metabolic network. Transcriptome analysis of human LIRI samples indicated disorder of fatty acid oxidation and mitochondrial homeostasis disruption. Within this pathway, hydroxyacyl-CoA dehydrogenase (HADH), a key mitochondrial β-oxidation enzyme, was identified as a potential biomarker (AUC = 0.79). In Sprague-Dawley (SD) rats exposed to 60-min ischemia and 2-h reperfusion (I/R), the pulmonary expression of HADH decreased by about 50%. HADH overexpression mediated by adenoviruses conferred multi-faceted pulmonary protection both in vivo and in vitro: in I/R-subjected SD rats, it alleviated mitochondrial impairment, boosted ATP production, diminished ROS levels, and limited alveolar apoptosis; these effects were corroborated in RLE-6TN AT2 cells exposed to 2-h hypoxia/4-h reoxygenation (H/R). Building on evidence that lysine succinylation modulates mitochondrial enzyme activity, we further identified 7 succinylated lysine residues within the catalytic domain of HADH-rather than its dimerization domain-highlighting its potential functional significance. Specifically, 3-oxoacid CoA-transferase 1 (OXCT1) increased HADH succinylation at lysine 81 (K81), stabilizing HADH by blocking its degradation via chaperone-mediated autophagy (CMA). The activated OXCT1-HADH axis reduced non-esterified fatty acid accumulation. OXCT1-succinylated K81 disrupted binding between HADH and heat shock protein A8 (HSPA8), a CMA recognition factor. HADH has a canonical HSPA8-binding CMA motif; mutating its key glutamine (Q132) or silencing HSPA8 inhibited CMA-mediated HADH degradation. Virtual screening shows that small-molecule drugs binding to HSPA8's active pocket (near its interaction region with HADH K81) have potential in treating post-lung transplantation dysfunction. Our findings elucidate the succinylation-dependent regulatory mechanism of HADH and provide a potential therapeutic strategy for LIRI. - Source: PubMed
Publication date: 2026/02/28
Li JiweiGuan HeMiao PengHan ZhijunDing ChengzhiJin ZheWei Li - Obesity and its associated metabolic disorders pose a major global health challenge. Theaflavins (TFs), bioactive polyphenols derived from black tea, have demonstrated potential in alleviating metabolic diseases. This study aimed to investigate the ameliorative effects and underlying mechanisms of TFs on high-fat diet (HFD)-induced obesity from the perspectives of oxidative stress, the branched-chain amino acid (BCAA) degradation pathway, and the gut microbiota. , TFs exhibited potent free-radical scavenging capacity. , TFs dose-dependently attenuated HFD-induced weight gain, dyslipidemia and glucose intolerance. Concurrently, TF administration alleviated hepatic steatosis and ultrastructural damage and improved liver function. Importantly, TFs suppressed hepatic oxidative stress and downregulated the HFD-induced overexpression of the valine, leucine, and isoleucine degradation pathway at both mRNA and protein levels (HADH, HMGCL, ACSF3, ACADS, ALDH3A2, and ACAA2). Furthermore, gut microbiota analysis revealed that TFs improved HFD-induced gut dysbiosis, characterized by the enrichment of butyrate-producing genera (, and ) and a reduction in the relative abundance of harmful taxa (, and ). Correlation analysis integrated these findings, revealing significant associations between the TF-induced microbial shifts, the ameliorated metabolic phenotypes, and the suppressed hepatic BCAA catabolism. Our study demonstrated that the alleviation of obesity by TFs was associated with multifaceted improvements, including enhanced antioxidant capacity, amelioration of dysregulated hepatic BCAA catabolism, and modulation of gut microbial homeostasis, highlighting their potential as a dietary intervention for metabolic diseases. - Source: PubMed
Publication date: 2026/03/09
Pan RuiliWu PingZhang YifanShi XiaoleiZhang YuGu DajiangZhao Jin