Ask about this productRelated genes to: PYGL antibody
- Gene:
- PYGL NIH gene
- Name:
- glycogen phosphorylase L
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-13
Related products to: PYGL antibody
Related articles to: PYGL antibody
- Acute myocardial infarction (AMI) is a major global health burden. Current diagnostic reliance on high-sensitivity cardiac troponin (hs-cTn) is limited by its lack of disease specificity and inability to reveal upstream molecular and immune mechanisms. This study aimed to identify robust core genes and their functional networks in AMI via integrated multi-dataset analysis and experimental validation. Three peripheral blood transcriptomic datasets (GSE60993, GSE61144, GSE97320) were obtained from GEO. Differentially expressed genes (DEGs) were identified using limma, with common DEGs extracted. Diagnostic performance was evaluated via ROC curves. Functional annotation used GO, KEGG and GSEA. Immune infiltration was analyzed with CIBERSORT. Key genes were validated in H9C2 cells under oxygen-glucose deprivation (OGD) using RT-qPCR and Western blot. Eight core genes were consistently upregulated in AMI peripheral blood, all showing high diagnostic accuracy (AUC > 0.80). They were enriched in immune-inflammatory pathways. GSEA identified three activated pathways: adipocytokine signaling, leukocyte transendothelial migration and insulin signaling, with ACSL1, MMP9 and PYGL as key drivers. Immune analysis revealed increased neutrophils and decreased γδ T cells, with all eight genes positively correlating with neutrophil infiltration. The OGD model in H9C2 cells confirmed specific upregulation of GPR97, PROK2, ALPL and PADI4. This integrated computational and experimental study identifies a set of high-value diagnostic core genes in AMI. It first validates the specific upregulation of novel genes (GPR97, PROK2) in myocardial ischemia, placing them within a pathological network involving metabolic, immune and protective pathways. These findings provide new molecular insights and a foundation for novel diagnostics and therapeutic targets. - Source: PubMed
Publication date: 2026/08/10
Meng YuminChen QifanLiu Jie - This study investigates the molecular mechanisms of renal clear cell carcinoma (RCC) induced by Aristolochic acid A (AAA) using machine learning, deep learning, and molecular docking approaches. - Source: PubMed
Publication date: 2026/07/20
Li LongzhuLiao JiachengChen XintianLin ZeqiongGong SiqiaoHuang JunminBi ZiqianWang TianyangChia XinliangChen LuXu YongzhiLiu HuafengHao JunfengQi Jiansong - As the cheapest feed ingredient, carbohydrates exert a protein-sparing effect. However, excessive carbohydrate intake can induce hepatic metabolic disorders and lead to metabolic diseases in fish. The GIP/GIPR axis plays a vital role in regulating lipid metabolism and glucose uptake. To evaluate the functions of GIP and GIPR in largemouth bass, we cloned their cDNA sequences. We analysed the tissue-specific expression of both genes and assessed the role of GIP in regulating glucose and lipid metabolism using hepatocyte studies and GIP interference assays. The largemouth bass gip gene (318 bp) encodes a protein of 105 amino acids, whereas the gipr gene (1614 bp) encodes a protein of 537 amino acids. Tissue distribution analysis revealed high expression of gip mRNA in the stomach. Additionally, gipr mRNA was highly expressed in the brain, foregut, midgut and hindgut. Both high-carbohydrate and high-fat intake in largemouth bass resulted in higher gip mRNA in the stomach and lower gipr mRNA expression in the foregut. Primary hepatocyte experiments showed that GIP treatment increased the expression of g6pase, acc1 and fas and decreased the expression of gk, pfk, hsl and lpl. Intraperitoneal injection of GIP small interfering RNA (siRNA) demonstrated that inhibiting GIP expression significantly reduced serum glucose and triglyceride levels. It also decreased the hepatic expression of g6pase, fbp1, pygl, acc1, fas and lpl, while increasing the expression of gys2 and hsl. These results suggest that GIP and GIPR regulate glucose and lipid metabolism in largemouth bass. - Source: PubMed
Publication date: 2026/07/18
Yin MingyueGuo ShihuiGu JianingZhang YingYang LiliZhang YanminZhang XindangChang XuluFeng ShikunNaiel Mohammed A EYang GuokunMeng Xiaolin - Aberrant metabolic alterations underlie microglial dysfunction, which plays an important role during neurodegenerative progression. However, the role of aberrant glycogen metabolism remains elusive. Here, we identified glycogen accumulation and upregulated glycogenolytic enzymes in brain microglia from patients with Alzheimer's disease (AD) and transgenic animal models. Particularly, the principal microglial glycogenolytic enzyme PYGL exhibited the most notable spatiotemporal upregulation during disease progression. Specific knockdown of microglial PYGL ameliorated neuropathological changes and cognitive deficits in AD mice. Bioinformatics analysis and experimental validation confirmed that enhancing microglial autophagic flux-dependent A clearance was the underlying mechanism. Furthermore, among all possible glycogenolytic pathways, PYGL downregulation primarily reduced hexosamine biosynthesis pathway activity, diminished UDP-GlcNAc and -GlcNAcylation of the autophagy key protein SNAP29, and thereby facilitated formation of the SNARE complex, which is essential for autophagosome-lysosome fusion. These findings reveal a glycogenolysis-driven post-translational pathway regulating microglial autophagy, establishing PYGL as a therapeutic target for AD. - Source: PubMed
Publication date: 2026/04/27
Ding YiLi Shi-YaoZhang Wen-FengChu Mao-MaoWang Xue-JieZhang Yu-GeZhang Hui-WenZhang Yu-TongXu LuLiu XueMorita TsuyoshiBaba OttoRen Zi-JianZhang Yong-JieZhang Zhi-YuanLi Lei - Most spinal muscular atrophy (SMA) patients develop severe scoliosis by late adolescence. Given that the paraspinal muscles-particularly the multifidus-are indispensable for maintaining spinal stability, their site-specific multi-omics characteristics in SMA remain insufficiently defined. Herein, integrated multi-omics sequencing was performed on bilateral multifidus samples from SMA patients and surgical controls. We identified 5219 differentially expressed genes, 1063 differentially expressed proteins and 370 differential metabolites between the control and SMA, showing significant enrichment in glucose and amino acid metabolism pathways, specifically key steps of glycolysis/gluconeogenesis. Key enzymes in the glycolytic process such as PFKM, ENO3 and PKM1 were markedly downregulated. Notably, a comparative analysis of the bilateral paraspinal muscles in SMA revealed asymmetrical metabolic signatures in carbohydrate and amino acid processing between the concave and convex sides. Key regulatory enzymes exhibited significant differential expression: PYGL, a central driver of starch and sucrose metabolism; creatine kinase, involved in arginine and proline metabolism; and PGAM2, a key mediator of glycine, serine, and threonine metabolism. These metabolic signatures indicate a complex metabolic reprogramming in the multifidus, where asymmetric disparities point to the influence of mechanical loading, while systemic dysregulation aligns with the effects of SMN depletion. - Source: PubMed
Wang ZhenZhao JunduoHuang Xu'anChen WeiyunShen Jianxiong