Ask about this productRelated genes to: PYGB protein
- Gene:
- PYGB NIH gene
- Name:
- glycogen phosphorylase B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-27
- Date modifiied:
- 2016-10-13
Related products to: PYGB protein
Related articles to: PYGB protein
- Weight-loss treatment is crucial for individuals with obesity to prevent various complications. The role of Immune cells in obesity has been recently recognized, whereas its translation into therapy requires identifying key target genes. We performed Mendelian randomization (MR) analysis to assess causal relationships between expression quantitative trait loci (eQTL) of 14 immune cells and obesity-related traits (obesity, body mass index and body fat percentage), and validated the results in colocalization analysis. For the putative causal genes identified by the MR and colocalization analyses, we conducted pathway enrichment, differential expressed gene (DEG) analysis and search of druggable evidence, and utilized a Tier system to prioritize drug targets for obesity. MR and colocalization evidence was observed for 1630 genes associated with one or more obesity-related traits, mainly expressed in CD4 naive/central memory T cells and enriched in antigen processing and presentation pathways. Forty-one genes showed causal relationship with all three outcomes, among which 19 genes have not been reported for obesity previously. DEG analysis using single-cell RNA sequencing data of blood or adipose tissue indicated that the differential expression of UBE2Z in monocytes, ZCCHC7 in T cells, and FNBP4 in B cells between lean and obese individuals were consistent with the MR results. By searching drug-gene interaction databases, we found targeted drugs for PYGB and PRUNE1, and PYGB was the top gene ranked in the Tier system. This study provides evidence for the involvement of immune cells in obesity, and the potential cell-specific, immune-related targets for obesity treatment. - Source: PubMed
Zhang XingjianTian YongRen XiaoyingTian JuanLiu JiaWang Guang - Chronic pain remains a major unmet medical challenge, yet the metabolic checkpoints that govern its persistence are poorly defined. Astrocytes are increasingly recognized as chemically programmable hubs that tune neuronal excitability through metabolic circuits. Building on reports that astrocyte-neuron lactate shuttling (ANLS) in the anterior cingulate cortex (ACC) supports chronic pain, we asked how astrocytic metabolic states evolve over the course of pain chronification. Using untargeted metabolomics of the ACC combined with GFAP-RiboTag-based astrocyte-specific transcriptomics, we provide a time-resolved map of astrocytic metabolism across the transition from acute nociception to chronic neuropathic pain. This analysis reveals a biphasic glycogen program-an acute glycogenolysis-triggered glycogen supercompensation-that culminates in the emergence of a Warburg-like metabolic signature associated with late astrocyte-enriched glycolytic and lactate-related changes and persistent circuit activation. Using glycogen phosphorylase inhibitors (GPI-1, GPI-2) as pharmacological probes, we show that early glycogenolysis blockade attenuates this Warburg-like shift, partially normalizes ACC metabolic signatures, and reduces long-lasting mechanical hypersensitivity, without impairing acute nociceptive sensitization. These findings identify astrocytic metabolic reprogramming as a pharmacologically tractable circuit-level process and nominate glycogenolysis as an upstream biochemical gate and potential therapeutic control point in neuropathic pain. - Source: PubMed
Publication date: 2026/05/02
Park Jun SeoKim Kwang HwanJun Hye WonChoi Se-YoungPark Seung BumLee Sung Joong - Glycolytic reprogramming has been implicated in rheumatoid arthritis (RA) pathogenesis, yet the underlying causal genes and epigenetic mechanisms remain unclear. This study aimed to systematically identify glycolysis-related genes and their methylation-regulated expression that may causally influence RA susceptibility. - Source: PubMed
Publication date: 2026/01/22
A XinyuXin PengfeiZheng LinXu BoWang JianyeSun SongtaoXie JunGao ChenxinPan PeijunQiu GuoweiJin LangShen JunXu XiruiCheng YiweiPei ShaoqiangRan LeiBian YanqinXiao Lianbo - In aged humans and mice, hypobranched glycogen aggregates, known as polyglucosan bodies (PGBs), accumulate in hippocampal astrocytes. While PGBs are linked to cognitive decline in neurological diseases, they remain largely unstudied in the context of typical aging. We show that PGBs arise in autophagy-dysregulated astrocytes in the aged hippocampus, with substantial variation among 32 inbred BXD mouse strains. Genetic mapping through quantitative trait locus analysis identified a major locus (Pgb1) that modulates hippocampal PGB burden. Extensive transcriptomic and proteomic datasets were produced for the aged hippocampus of the BXD family to investigate the mechanism by which the Pgb1 locus modulates PGB burden. We identified that Pgb1 contains allelic Smarcal1 and Usp37 variants and influences PGB burden through trans-regulation of mRNA and protein expression levels, including abundance of glycogen-mobilizing factor PYGB. Furthermore, comprehensive phenome-wide association scans, transcriptomic analyses, and direct behavioral testing demonstrated that cognition remains intact despite age-related PGB burden. A record of this paper's transparent peer review process is included in the supplemental information. - Source: PubMed
Publication date: 2026/02/02
Gómez-Pascual AliciaGlikman Dow MNg Hui XinTomkins James ELu LuXu YingAshbrook David GKaczorowski CatherineKempermann GerdKillmar JohnMozhui KhyobeniOhlenschläger OliverAebersold RudolfIngram Donald KWilliams Evan GJucker MathiasOverall Rupert WWilliams Robert Wde Bakker Dennis E M - Lung squamous cell carcinoma (LUSC) is a common and aggressive malignancy. Necroptosis, a regulated mode of cell death, has been implicated in tumor immunity and oncogenic processes, yet the mechanistic involvement of necroptosis-related genes (NRGs) in LUSC pathogenesis remains unclear, necessitating systematic evaluation of their biological and clinical relevance. - Source: PubMed
Publication date: 2025/10/29
Sun KaiWang Ke-RunWen SongHong Juan-JuanFei Yu-LangPan Qing-HuaXie Fang-Fang