Ask about this productRelated genes to: HMGCL Blocking Peptide
- Gene:
- HMGCL NIH gene
- Name:
- 3-hydroxy-3-methylglutaryl-CoA lyase
- Previous symbol:
- -
- Synonyms:
- HL
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-13
- Date modifiied:
- 2018-05-29
Related products to: HMGCL Blocking Peptide
Related articles to: HMGCL Blocking Peptide
- Hepatocellular carcinoma (HCC) is a major type of primary liver cancer. Previous studies have reported that interleukin enhancer-binding factor 3 (ILF3) is involved in the regulation of multiple cancers. This study investigated the molecular mechanisms whereby ILF3 promotes HCC progression. - Source: PubMed
Publication date: 2026/04/29
Luo QingqingXiao LeiDeng GanluDeng TanZhao WenchaoWang RenshengHu Xueying - Zinc finger protein 460 (ZNF460) is highly expressed in colon cancer, but its specific mechanism of action and downstream targets have not yet been clarified. Therefore, this study aimed to investigate the expression pattern, prognostic value, and biological function of ZNF460 in colorectal cancer (CRC), and to elucidate its underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/03/24
Hou WenpeiWang JiaWu YuqiangLi ZhengguoXu KeruiHan XiaZhang LianxingLi YanLi Zhihu - This study aimed to examine the clinical characteristics of Chinese patients with 3-hydroxy-3-methylglutaryl-CoA lyase deficiency (HMGLD) and identify the prevalent mutations in the gene among these patients. - Source: PubMed
Publication date: 2026/03/23
Yang KunZhang YuandaZang LiliLiu YingLi YajuanWang WenhuanZhang PingZhao ZeTian LeiLiu Jingxia - The ketogenic process has been reported to play an important role in human pathophysiology and may contribute to the treatment of psychotic disorders. Increased plasma ketone body β-hydroxybutyrate (BHB) levels were observed under the intervention of risperidone with voluntary exercise. Since BHB in the brain originates from both plasma and astrocytic production and plays a neuroprotective role, this study investigated the effects of risperidone and/or voluntary exercise on the expression of genes related to ketone body synthesis, degradation, and transport in the hippocampus and prefrontal cortex (PFC), specifically focusing on mechanisms underlying cerebral BHB production. - Source: PubMed
Publication date: 2026/03/05
Yi WeijieLian JiameiDeng Chao - 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