Recombinant Human Acetyl-COA Acyltransferase ACAA1
- Known as:
- Recombinant Human Acetyl-COA Acyltransferase ACAA1
- Catalog number:
- enz-251
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Acetyl-COA Acyltransferase ACAA1
Ask about this productRelated genes to: Recombinant Human Acetyl-COA Acyltransferase ACAA1
- Gene:
- ACAA1 NIH gene
- Name:
- acetyl-CoA acyltransferase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-03-22
Related products to: Recombinant Human Acetyl-COA Acyltransferase ACAA1
Related articles to: Recombinant Human Acetyl-COA Acyltransferase ACAA1
- Heat stress leads to excessive hepatic lipid deposition and oxidative imbalance in laying hens, especially during peak laying period. Chlorogenic acid (CGA), a dietary polyphenol with antioxidant and lipid-modulating properties, may improve hepatic lipid homeostasis, yet its effects under heat-stress conditions remain unclear. In this study, 240 Hy-Line Brown laying hens at 36 weeks of age were randomly assigned to one of two treatments (120 hens per treatment, with six replicates of 20 hens each): a basal diet or a basal diet supplemented with 300 mg/kg CGA and subjected to heat-stress conditions for 8 weeks. CGA supplementation significantly reduced liver weight (25.3%), liver index (14.4%), hepatic triglyceride content (29.1%), and serum triglyceride level (61.7%) ( < 0.05). Histological assessment revealed lower steatosis and inflammation scores, alongside increased hepatic SOD activity (13.6%) and decreased MDA content (58.7%) ( < 0.05). RNA-seq analysis identified 420 differentially expressed genes that were significantly enriched in PPAR signaling and fatty acid β-oxidation pathways. CGA upregulated fatty acid oxidation-related genes (, , , ) and downregulated lipogenic markers (, ). Serum metabolomics revealed coordinated changes in lipid and carbon metabolism. These results indicate that dietary CGA alleviates hepatic lipid accumulation and oxidative stress in heat-stressed peak-laying hens, potentially via PPARα-mediated enhancement of fatty acid oxidation and inhibition of de novo lipogenesis. - Source: PubMed
Publication date: 2026/06/12
Wang DanTan HaiqiuPeng LinWu XuanfuGao JiangMa Wenqiang - Crystal adhesion is a key process in the formation of kidney stones, playing a synergistic role at every crystallization stage. Damage to the renal tubular epithelial cell (RTEC) membrane provides essential sites for crystal adhesion. During the terminal phase of ferroptosis, accumulated polyunsaturated phospholipids integrate into the cell membrane, leading to membrane damage and deformation, which may be an important mechanism in calcium oxalate (CaOx) crystallization. In this study, targeted peroxidomics analysis revealed a significant increase in arachidonic acid (AA) levels in a CaOx kidney stone model. Meanwhile, transcriptomic analysis indicated that the key enzyme in fatty acid metabolism, acetyl-coenzyme A (CoA) acyltransferase 1 (ACAA1), was significantly downregulated in the CaOx kidney stone model. Besides, overexpression of ACAA1 (OE-ACAA1) alleviated AA accumulation and reduced oxalate (Ox)-induced RTEC ferroptosis. Notably, the OE-ACAA1 alleviated the accumulation of AA-containing polyunsaturated phospholipids without regulating acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, thereby reducing membrane peroxidative damage and crystal adhesion. Furthermore, transcription factor array analysis identified the downregulation of activating transcription factor 1 (ATF1), an upstream transcriptional regulator of ACAA1, which might be involved in the transcriptional repression of ACAA1. Finally, OE-ATF1 partially alleviated Ox-induced RTEC membrane peroxidative damage and crystal adhesion. These findings demonstrated that ferroptosis participates in the early crystallization process by mediating RTEC membrane peroxidative damage and provided a novel approach to influencing downstream lipid peroxidation by regulating fatty acid activation substrates rather than ACSL4. Therefore, this study offers potential therapeutic targets for the prevention and treatment of CaOx kidney stones. - Source: PubMed
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