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
- Genetic variants associated with stroke prognosis remain poorly characterized at the functional level. Here, we integrated summary-data-based Mendelian randomization with brain expression quantitative trait locus data, Bayesian colocalization, and cell-type-specific analyses to identify causal genes for functional outcome measured by the modified Rankin Scale at three months post-ischemic stroke. We identified four genes with robust evidence: PYGL, GSTA1, and PTGIS as protective factors, and NFATC1 as a risk factor. Cell-type-specific analyses revealed that PYGL exerts its protective effect primarily through excitatory neurons, while the detrimental effect of NFATC1 is specific to oligodendrocytes. Mediation analyses demonstrated that white matter tract integrity and cortical thickness partially mediate the associations between these genes and stroke outcomes. Functional validation in hippocampal neuronal cells confirmed that PYGL overexpression significantly attenuated apoptosis induced by oxygen-glucose deprivation/reperfusion, whereas PYGL silencing exacerbated injury. These findings delineate a causal gene regulatory network underlying stroke prognosis, highlight the importance of neuronal energy metabolism and oligodendrocyte function in recovery, and nominate PYGL as a potential therapeutic target for promoting functional recovery after ischemic stroke. - Source: PubMed
Publication date: 2026/09/15
Li KeYuan HuiZhou Dayong - Hepatitis E virus (HEV) is a significant cause of acute liver failure (ALF). The role of glycogen phosphorylase L (PYGL) in the diagnosis and prognosis of HEV-ALF remains unclear. This study collected clinical data and baseline characteristics from HEV-ALF patients, acute hepatitis E (AHE) patients, and healthy controls (HCs), measuring serum PYGL levels in each group. Methods including Orthogonal partial least squares discriminant analysis (OPLS-DA), receiver operating characteristic (ROC) and decision curve analysis (DCA) were used to evaluate the clinical utility of PYGL. Results showed that PYGL effectively diagnosed HEV-ALF (AUC = 0.911). PYGL levels were significantly higher in HEV-ALF patients than in AHE patients and HCs (p < 0.001). Among HEV-ALF patients, non-survivors exhibited higher PYGL levels than survivors (p < 0.001). PYGL demonstrated good predictive ability for 30-day mortality (AUC = 0.859). OPLS-DA and DCA confirmed its strong decision-making utility. Furthermore, PYGL levels escalated with increasing organ failure and paralleled clinical worsening, being highest in the deterioration group (p < 0.05). PYGL is a potential diagnostic and prognostic biomarker in HEV-ALF patients, where elevated levels indicate poorer outcomes and support early intervention. - Source: PubMed
Feng SiyuPan MingzhiWang LuyuJi ChangyiXiang ZeWu JianGu Mengmeng - Coronary heart disease (CHD) is a leading cause of morbidity and mortality, driven by metabolic remodeling, vascular inflammation, and perivascular adipose tissue (PVAT) dysfunction. We integrated bulk transcriptomic datasets to develop a machine learning-based diagnostic model, evaluated 113 algorithms, and identified a seven-gene signature (, , , , , , ) with robust predictive performance. Single-cell RNA sequencing (scRNA-seq) of coronary PVAT revealed substantial cellular heterogeneity and prioritized PFKFB3 as a hub linking glycolytic activity to nuclear factor kappa B (NF-κB) regulon activity. Macrophage-centered communication via secreted phosphoprotein 1 (SPP1), migration inhibitory factor (MIF), and other pathways was enhanced in disease conditions. Virtual knockout of PFKFB3 induced transcriptional changes enriched in immune activation, phagocytosis, and oxidative stress, while molecular dynamics (MD) simulations suggested that salidroside can adopt a stable binding pose within the PFKFB3 pocket, providing structural plausibility for their interaction. Together, these analyses provide a multi-layered framework connecting glycolytic remodeling, inflammatory transcriptional activity, and intercellular signaling in CHD. The findings support PFKFB3 as a potential biomarker and mechanistic hub and suggest that salidroside may modulate its activity. This study offers an integrative computational foundation for future experimental validation and mechanistic exploration of PVAT dysfunction in CHD. - Source: PubMed
Publication date: 2026/08/19
Yang HaoboZhang YonghuiYu YunfengBai YananZhu JialeChen OuyingWang LipingJian Weixiong - 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